Growth in Disorders of Adrenal Hyperfunction
Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 ± 0.42 and 1.3 ± 0.37 SDS respectively. In poorly contr...
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Published in | Hormone research Vol. 58; no. Suppl 1; pp. 39 - 43 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Basel, Switzerland
01.01.2002
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Subjects | |
Online Access | Get full text |
ISBN | 9783805574754 3805574754 |
ISSN | 1663-2818 0301-0163 1663-2826 |
DOI | 10.1159/000064767 |
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Abstract | Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 ± 0.42 and 1.3 ± 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m 2 /day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4–17.8 years, with Cushing’s disease (CD). At diagnosis, mean height SDS was –1.81 (1.2 to –4.17), 53% < –1.8 SDS, height velocity in 6 was 0.9–3.8 cm/year and mean BMI SDS 2.29 (0.7–5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1–108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10–29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 ± 3.4 years, growth after cure was studied for 9.1 ± 5.0 years. Nine had no catch-up growth in the interval of 0.3–1.1 years after cure (mean HV 5.3 ± 2.4 cm/year). All these had GH deficiency peak GH 0.5–20.9 mU/l, and received hGH 2.7 mg/m 2 /week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS–target Ht SDS) –1.72 ± 1.26 improving to –0.83 ± 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (–2.9 to 3.0), –0.8 (6.0 to 2.2), 0.7 (–7.9 to 9.5) respectively, whereas SHBG was reduced at –2.1 (–5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height. |
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AbstractList | Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 ± 0.42 and 1.3 ± 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m2/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4–17.8 years, with Cushing’s disease (CD). At diagnosis, mean height SDS was –1.81 (1.2 to –4.17), 53% < –1.8 SDS, height velocity in 6 was 0.9–3.8 cm/year and mean BMI SDS 2.29 (0.7–5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1–108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10–29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 ± 3.4 years, growth after cure was studied for 9.1 ± 5.0 years. Nine had no catch-up growth in the interval of 0.3–1.1 years after cure (mean HV 5.3 ± 2.4 cm/year). All these had GH deficiency peak GH 0.5–20.9 mU/l, and received hGH 2.7 mg/m2/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS–target Ht SDS) –1.72 ± 1.26 improving to –0.83 ± 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (–2.9 to 3.0), –0.8 (6.0 to 2.2), 0.7 (–7.9 to 9.5) respectively, whereas SHBG was reduced at –2.1 (–5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height. Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 ± 0.42 and 1.3 ± 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m 2 /day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4–17.8 years, with Cushing’s disease (CD). At diagnosis, mean height SDS was –1.81 (1.2 to –4.17), 53% < –1.8 SDS, height velocity in 6 was 0.9–3.8 cm/year and mean BMI SDS 2.29 (0.7–5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1–108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10–29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 ± 3.4 years, growth after cure was studied for 9.1 ± 5.0 years. Nine had no catch-up growth in the interval of 0.3–1.1 years after cure (mean HV 5.3 ± 2.4 cm/year). All these had GH deficiency peak GH 0.5–20.9 mU/l, and received hGH 2.7 mg/m 2 /week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS–target Ht SDS) –1.72 ± 1.26 improving to –0.83 ± 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (–2.9 to 3.0), –0.8 (6.0 to 2.2), 0.7 (–7.9 to 9.5) respectively, whereas SHBG was reduced at –2.1 (–5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height. Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 +/- 0.42 and 1.3 +/- 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m(2)/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4-17.8 years, with Cushing's disease (CD). At diagnosis, mean height SDS was -1.81 (1.2 to -4.17), 53% < -1.8 SDS, height velocity in 6 was 0.9-3.8 cm/year and mean BMI SDS 2.29 (0.7-5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1-108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10-29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 +/- 3.4 years, growth after cure was studied for 9.1 +/- 5.0 years. Nine had no catch-up growth in the interval of 0.3-1.1 years after cure (mean HV 5.3 +/- 2.4 cm/year). All these had GH deficiency peak GH 0.5-20.9 mU/l, and received hGH 2.7 mg/m(2)/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS-target Ht SDS) -1.72 +/- 1.26 improving to -0.83 +/- 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (-2.9 to 3.0), -0.8 (6.0 to 2.2), 0.7 (-7.9 to 9.5) respectively, whereas SHBG was reduced at -2.1 (-5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height.Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 +/- 0.42 and 1.3 +/- 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m(2)/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4-17.8 years, with Cushing's disease (CD). At diagnosis, mean height SDS was -1.81 (1.2 to -4.17), 53% < -1.8 SDS, height velocity in 6 was 0.9-3.8 cm/year and mean BMI SDS 2.29 (0.7-5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1-108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10-29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 +/- 3.4 years, growth after cure was studied for 9.1 +/- 5.0 years. Nine had no catch-up growth in the interval of 0.3-1.1 years after cure (mean HV 5.3 +/- 2.4 cm/year). All these had GH deficiency peak GH 0.5-20.9 mU/l, and received hGH 2.7 mg/m(2)/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS-target Ht SDS) -1.72 +/- 1.26 improving to -0.83 +/- 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (-2.9 to 3.0), -0.8 (6.0 to 2.2), 0.7 (-7.9 to 9.5) respectively, whereas SHBG was reduced at -2.1 (-5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height. Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 +/- 0.42 and 1.3 +/- 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m(2)/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4-17.8 years, with Cushing's disease (CD). At diagnosis, mean height SDS was -1.81 (1.2 to -4.17), 53% < -1.8 SDS, height velocity in 6 was 0.9-3.8 cm/year and mean BMI SDS 2.29 (0.7-5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1-108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10-29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 +/- 3.4 years, growth after cure was studied for 9.1 +/- 5.0 years. Nine had no catch-up growth in the interval of 0.3-1.1 years after cure (mean HV 5.3 +/- 2.4 cm/year). All these had GH deficiency peak GH 0.5-20.9 mU/l, and received hGH 2.7 mg/m(2)/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS-target Ht SDS) -1.72 +/- 1.26 improving to -0.83 +/- 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (-2.9 to 3.0), -0.8 (6.0 to 2.2), 0.7 (-7.9 to 9.5) respectively, whereas SHBG was reduced at -2.1 (-5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height. |
Author | Monson, J.P. Carroll, P.V. Ho, J.T.F. Besser, G.M. Grossman, A.B. Savage, M.O. Scommegna, S. |
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Cites_doi | 10.1210/jc.78.1.131 10.1056/NEJM199409083311002 10.1210/jc.79.4.1082 10.1159/000049990 |
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Keywords | Adrenal tumour Adrenal disease Congenital adrenal hyperplasia Growth Cushing's disease |
Language | English |
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PublicationYear | 2002 |
References | Salt AT, Savage MO, Grant DB: Growth patterns after surgery for virilizing adrenocortical adenoma. Arch Dis Child 1992;67:234-236.1311916 Magiakou MA, Mastorakos G, Oldfield EH, Gomez MR, Doppman JL, Cutler GB, Nieman LK, Chrousos GP: Cushing's syndrome in children and adolescents. Presentation, diagnosis and therapy. N Engl J Med 1994;331:629-636.805227210.1056/NEJM199409083311002 Magiakou MA, Mastorakos G, Chrousos GP: Final stature in patents with endogenous Cushing's syndrome. J Clin Endocrinol Metab 1994;79:1082-1085.796227710.1210/jc.79.4.1082 Thilén A, Woods KA, Perry LA, Savage MO, Wedell A, Ritzén EM: Early growth is not increased in untreated moderately severe 21-hydroxylase deficiency. Acta Pediatr 1995;84:894-898.7488813 Savage MO, Lienhardt A, Lebrethon MC, Johnston LB, Huebner A, Grossman AB, Afshar F, Plowman PN, Besser GM: Cushing's disease in childhood: Presentation, investigation, treatment and long-term outcome. Horm Res 2001;55(suppl 1):24-30. Hargitai G, Sólyom J, Battelino T, Lebl J, Pribilincová F, Frisch H and MEWPE-CAH Study Group: Growth patterns and final height in congenital adrenal hyperplasia due to classical 21-hydroxylase deficiency. Horm Res 2001;55:161-171.1159836910.1159/000049990 Balakumar T, Perry LA, Savage MO: Adrenocortical adenoma - An unusual presentation with hypersecretion of oestradiol, androgens and cortisol. J Pediatr Endocrinol Metab 1997;10:227-229. Ho JFT, Blair JC, Perry LA, Lienhardt A, Ong K, Dunger DB, Grossman AB, Besser GM, Savage MO: Evolution of serum androstenedione, DHEA-S, testosterone and SHBG concentrations at diagnosis and following treatment of paediatric Cushing's diseaes. Pediatr Res 2001;49(suppl):P1-722. Honour JW, Price DA, Taylor NF, Marsden HB, Grant DB: Steroid biochemistry of virilising adrenal tumours in childhood. Eur J Pediatr 1984;142:156-159. Urban MD, Lee PA, Migeon CJ: Adult height and fertility in men with congenital virilizing adrenal hyperplasia. N Engl J Med 1978;299:1392-1396.152409 Clayton G: Patterns of growth from birth to maturity in infants and children with congenital adrenal hyperplasia. Acta Endocrinol 1986;113:295-304. Lebrethon MC, Grossman AB, Afshar F, Plowman PB, Bessre GM, Savage MO: Linear growth and final height after treatment for Cushing's disease in childhood. J Clin Endocrinol Metab 2000;85:3262-3265.10999819 Jääskeläinen J, Voutilainen R: Growth of patients with 21-hydroxylase deficiency: An analysis of the factors influencing adult height. Pediatr Res 1977;41:30-33. Wolthers OD, Cameron FJ, Scheimberg I, Honour JW, Hindmarsh PC, Savage MOS, Stanhope RG, Brook CGD: Androgen-secreting adrenocortical tumours. Arch Dis Child 1999;80:46-50.10325758 Carroll PV, Monson JP, Grossman AB, Plowman PN, Afshar F, Besser GM, Savage MO: Successful treatment of childhood Cushing's disease is associated with ongoing reduction in growth hormone secretion. Pediatr Res 2001;49(suppl):P1-49. Weber A, Trainer PJ, Grossman AB, Afshar F, Medbak S, Perry LA, Plowman PN, Rees LA, Besser GM, Savage MO: Investigation, management and therapeutic outcome in 12 cases of childhood and adolescent Cushing's syndrome. Clin Endocrinol 1995;43:19-28. Magiakou MA, Mastorakos G, Gomez MT, Rose SR, Chrousos GP: Suppressed spontaneous and stimulated growth hormone secretion in patients with Cushing's disease before and after surgical care. J Clin Endocrinol Metab 1994;78:131-137.750711810.1210/jc.78.1.131 ref2 ref1 ref4 ref3 |
References_xml | – reference: Hargitai G, Sólyom J, Battelino T, Lebl J, Pribilincová F, Frisch H and MEWPE-CAH Study Group: Growth patterns and final height in congenital adrenal hyperplasia due to classical 21-hydroxylase deficiency. Horm Res 2001;55:161-171.1159836910.1159/000049990 – reference: Weber A, Trainer PJ, Grossman AB, Afshar F, Medbak S, Perry LA, Plowman PN, Rees LA, Besser GM, Savage MO: Investigation, management and therapeutic outcome in 12 cases of childhood and adolescent Cushing's syndrome. Clin Endocrinol 1995;43:19-28. – reference: Thilén A, Woods KA, Perry LA, Savage MO, Wedell A, Ritzén EM: Early growth is not increased in untreated moderately severe 21-hydroxylase deficiency. Acta Pediatr 1995;84:894-898.7488813 – reference: Wolthers OD, Cameron FJ, Scheimberg I, Honour JW, Hindmarsh PC, Savage MOS, Stanhope RG, Brook CGD: Androgen-secreting adrenocortical tumours. Arch Dis Child 1999;80:46-50.10325758 – reference: Jääskeläinen J, Voutilainen R: Growth of patients with 21-hydroxylase deficiency: An analysis of the factors influencing adult height. Pediatr Res 1977;41:30-33. – reference: Urban MD, Lee PA, Migeon CJ: Adult height and fertility in men with congenital virilizing adrenal hyperplasia. N Engl J Med 1978;299:1392-1396.152409 – reference: Clayton G: Patterns of growth from birth to maturity in infants and children with congenital adrenal hyperplasia. Acta Endocrinol 1986;113:295-304. – reference: Ho JFT, Blair JC, Perry LA, Lienhardt A, Ong K, Dunger DB, Grossman AB, Besser GM, Savage MO: Evolution of serum androstenedione, DHEA-S, testosterone and SHBG concentrations at diagnosis and following treatment of paediatric Cushing's diseaes. Pediatr Res 2001;49(suppl):P1-722. – reference: Carroll PV, Monson JP, Grossman AB, Plowman PN, Afshar F, Besser GM, Savage MO: Successful treatment of childhood Cushing's disease is associated with ongoing reduction in growth hormone secretion. Pediatr Res 2001;49(suppl):P1-49. – reference: Magiakou MA, Mastorakos G, Oldfield EH, Gomez MR, Doppman JL, Cutler GB, Nieman LK, Chrousos GP: Cushing's syndrome in children and adolescents. Presentation, diagnosis and therapy. N Engl J Med 1994;331:629-636.805227210.1056/NEJM199409083311002 – reference: Balakumar T, Perry LA, Savage MO: Adrenocortical adenoma - An unusual presentation with hypersecretion of oestradiol, androgens and cortisol. J Pediatr Endocrinol Metab 1997;10:227-229. – reference: Lebrethon MC, Grossman AB, Afshar F, Plowman PB, Bessre GM, Savage MO: Linear growth and final height after treatment for Cushing's disease in childhood. J Clin Endocrinol Metab 2000;85:3262-3265.10999819 – reference: Salt AT, Savage MO, Grant DB: Growth patterns after surgery for virilizing adrenocortical adenoma. Arch Dis Child 1992;67:234-236.1311916 – reference: Honour JW, Price DA, Taylor NF, Marsden HB, Grant DB: Steroid biochemistry of virilising adrenal tumours in childhood. Eur J Pediatr 1984;142:156-159. – reference: Savage MO, Lienhardt A, Lebrethon MC, Johnston LB, Huebner A, Grossman AB, Afshar F, Plowman PN, Besser GM: Cushing's disease in childhood: Presentation, investigation, treatment and long-term outcome. Horm Res 2001;55(suppl 1):24-30. – reference: Magiakou MA, Mastorakos G, Gomez MT, Rose SR, Chrousos GP: Suppressed spontaneous and stimulated growth hormone secretion in patients with Cushing's disease before and after surgical care. J Clin Endocrinol Metab 1994;78:131-137.750711810.1210/jc.78.1.131 – reference: Magiakou MA, Mastorakos G, Chrousos GP: Final stature in patents with endogenous Cushing's syndrome. J Clin Endocrinol Metab 1994;79:1082-1085.796227710.1210/jc.79.4.1082 – ident: ref4 doi: 10.1210/jc.78.1.131 – ident: ref2 doi: 10.1056/NEJM199409083311002 – ident: ref3 doi: 10.1210/jc.79.4.1082 – ident: ref1 doi: 10.1159/000049990 |
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Snippet | Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9... |
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SubjectTerms | Adolescent Adrenal Gland Neoplasms - complications Adrenal Gland Neoplasms - physiopathology Adrenal Gland Neoplasms - therapy Adrenal Hyperplasia, Congenital - complications Adrenocortical Hyperfunction - complications Age Determination by Skeleton Androgens - blood Androgens - secretion Body Height Child Cushing Syndrome - complications Cushing Syndrome - physiopathology Cushing Syndrome - therapy Female Growth Disorders - etiology Human Growth Hormone - deficiency Humans Male |
Title | Growth in Disorders of Adrenal Hyperfunction |
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