Cited by 57Sexual Differentiation and DisordersAdrenal Hormones and DisordersOvarian function and disorders

Management of the female with non-classical congenital adrenal hyperplasia (NCCAH): a patient-oriented approach

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Livadas, Sarantis, Bothou, Christina·2019·Frontiers in Endocrinology

Abstract

Non-classical congenital adrenal hyperplasia (NCCAH) is considered to be a common monogenic inherited disease, with an incidence range from 1:500 to 1:100 births worldwide. However, despite the high incidence, there is a low genotype-phenotype correlation, which explains why NCCAH diagnosis is usually delayed or even never carried out, since many patients remain asymptomatic or are misdiagnosed as suffering from other hyperandrogenic disorders. For affected adolescent and adult women, it is crucial to investigate any suspicion of NCCAH and determine a firm and accurate diagnosis. The Synacthen test is a prerequisite in the event of clinical suspicion, and molecular testing will establish the diagnosis. In most cases occurring under 8 years of age, the first symptom is premature pubarche. In some cases, due to advanced bone age and/or severe signs of hyperandrogenism, initiation of hydrocortisone treatment prepubertally may be considered. Our unifying theory of the hyperandrogenic signs system and its regulation by internal (hormones, enzymes, tissue sensitivity) and external (stress, insulin resistance, epigenetic, endocrine disruptors) factors is presented in an attempt to elucidate both the prominent genotype-phenotype heterogeneity of this disease and the resultant wide variation of clinical findings. Treatment should be initiated not only to address the main cause of the patient's visit but additionally to decrease abnormally elevated hormone concentrations. Goals of treatment include restoration of regular menstrual cyclicity, slowing the progression of hirsutism and acne, and improvement of fertility. Hydrocortisone supplementation, though not dexamethasone administration, could, as a general rule, be helpful, however, at minimum doses, and also for a short period of time and, most likely, not lifelong. On the other hand, in cases where severe hirsutism and/or acne are present, prescription of oral contraceptives and/or antiandrogens may be advisable. Furthermore, women with NCCAH commonly experience subfertility, therefore, there will be analysis of the appropriate approach for these patients, including during pregnancy, based mainly on genotype. Besides, we should keep in mind that since the same patient will have changing requirements through the years, the attending physician should undertake a tailor-made approach in order to cover her specific needs at different stages of life.

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  • Supraphysiological dosages of glucocorticoids similar to those used to treat classic CAH patients may be necessary to suppress adrenal androgen production in NC CAH.

    “Supraphysiological dosages of glucocorticoids similar to those used to treat classic CAH patients may be necessary to suppress adrenal androgen production (426).”

    From Congenital Adrenal Hyperplasia—Current Insights in Pathophysiology, Diagnostics, and Management (2022) · cites this paper as [426]

    In “NCCAH Management From the First Manifestation to the Adult Life” (page unavailable), the paper says glucocorticoids are generally given at replacement, not pharmacological, doses to decrease adrenal androgen production. Its “Management During Childhood” section adds that very high doses are needed to suppress 17-OHP and progesterone, not that supraphysiological doses are necessary to suppress adrenal androgens. (LLM, conf=0.87)

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  1. [1]Speiser PW White PC. Congenital adrenal hyperplasia. N Engl J Med. (2003) 349: 776– 88. 10.1056/NEJMra021561 12930931 · DOI · Paper page
  2. [3]Speiser PW. Nonclassic adrenal hyperplasia. Rev Endocr Metab Disord. (2009) 10: 77– 82. 10.1007/s11154-008-9097-x 18690539 · DOI
  3. [5]Speiser PW Dupont B Rubinstein P Piazza A Kastelan A New MI. High frequency of nonclassical steroid 21-hydroxylase deficiency. Am J Hum Genet. (1985) 37: 650– 67. 9556656 PMC1684620
  4. [6]Wilson RC Nimkarn S Dumic M Obeid J Azar MR Azar M. Ethnic-specific distribution of mutations in 716 patients with congenital adrenal hyperplasia owing to 21-hydroxylase deficiency. Mol Genet Metab. (2007) 90: 414– 21. 10.1016/j.ymgme.2006.12.005 17275379 PMC1885892 · DOI
  5. [8]Witchel SF Azziz R. Nonclassic congenital adrenal hyperplasia. Int J Pediatr Endocrinol. (2010) 2010: 625105. 10.1186/1687-9856-2010-625105 20671993 PMC2910408 · DOI
  6. [10]White PC. Neonatal screening for congenital adrenal hyperplasia. Nat Rev Endocrinol. (2009) 5: 490– 8. 10.1038/nrendo.2009.148 19690561 · DOI · Paper page
  7. [12]Moran C Azziz R Carmina E Dewailly D Fruzzetti F Ibañez L. 21-Hydroxylase-deficient nonclassic adrenal hyperplasia is a progressive disorder: a multicenter study. Am J Obstet Gynecol. (2000) 183: 1468– 74. 10.1067/mob.2000.108020 11120512 · DOI · Paper page
  8. [14]Livadas S Dracopoulou M Dastamani A Sertedaki A Maniati-Christidi M Magiakou A-M. The spectrum of clinical, hormonal and molecular findings in 280 individuals with nonclassical congenital adrenal hyperplasia caused by mutations of the CYP21A2 gene. Clin Endocrinol (Oxf). (2015) 82: 543– 9. 10.1111/cen.12543 25041270 · DOI
  9. [15]Bidet M Bellanné-Chantelot C Galand-Portier M-B Tardy V Billaud L Laborde K. Clinical and molecular characterization of a cohort of 161 unrelated women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency and 330 family members. J Clin Endocrinol Metab. (2009) 94: 1570– 8. 10.1210/jc.2008-1582 19208730 · DOI · Paper page
  10. [16]Escobar-Morreale HF Sanchón R San Millán JL. A prospective study of the prevalence of nonclassical congenital adrenal hyperplasia among women presenting with hyperandrogenic symptoms and signs. J Clin Endocrinol Metab. (2008) 93: 527– 33. 10.1210/jc.2007-2053 18000084 · DOI
  11. [17]Dewailly D Vantyghem-Haudiquet MC Sainsard C Buvat J Cappoen JP Ardaens K. Clinical and biological phenotypes in late-onset 21-hydroxylase deficiency. J Clin Endocrinol Metab. (1986) 63: 418– 23. 10.1210/jcem-63-2-418 3013919 · DOI · Paper page
  12. [18]Gönç EN Ozön ZA Alikaşifoglu A Engiz O Bulum B Kandemir N. (2011). Is basal serum 17-OH progesterone a reliable parameter to predict nonclassical congenital adrenal hyperplasia in premature adrenarche? Turk J Pediatr. 53: 274– 80. 21980808
  13. [20]Dacou-Voutetakis C Dracopoulou M. High incidence of molecular defects of the CYP21 gene in patients with premature adrenarche. J Clin Endocrinol Metab. (1999) 84: 1570– 4. 10.1210/jc.84.5.1570 10323382 · DOI
  14. [21]Ambroziak U Kepczynska-Nyk A Kuryłowicz A Małunowicz EM Wójcicka A Miśkiewicz P. The diagnosis of nonclassic congenital adrenal hyperplasia due to 21-hydroxylase deficiency, based on serum basal or post-ACTH stimulation 17-hydroxyprogesterone, can lead to false-positive diagnosis. Clin Endocrinol (Oxf). (2016) 84: 23– 9. 10.1111/cen.12935 26331608 · DOI
  15. [22]Ambroziak U Kepczynska-Nyk A Kuryłowicz A Wysłouch-Cieszynska A Małunowicz EM Bartoszewicz Z. LC-MS/MS improves screening towards 21-hydroxylase deficiency. Gynecol Endocrinol. (2015) 31: 296– 300. 10.3109/09513590.2014.994599 25539143 · DOI
  16. [23]Keefe CC Goldman MM Zhang K Clarke N Reitz RE Welt CK. Simultaneous measurement of thirteen steroid hormones in women with polycystic ovary syndrome and control women using liquid chromatography-tandem mass spectrometry. PLoS One. (2014) 9: e93805. 10.1371/journal.pone.0093805 24713888 PMC3979722 · DOI
  17. [24]Ray JA Kushnir MM Yost RA Rockwood AL Wayne Meikle A. Performance enhancement in the measurement of 5 endogenous steroids by LC-MS/MS combined with differential ion mobility spectrometry. Clin Chim Acta. (2015) 438: 330– 6. 10.1016/j.cca.2014.07.036 25110813 · DOI · Paper page
  18. [25]Stoupa A González-Briceño L Pinto G Samara-Boustani D Thalassinos C Flechtner I. Inadequate cortisol response to the tetracosactide (Synacthen®) test in non-classic congenital adrenal hyperplasia: an exception to the rule? Horm Res Paediatr. (2015) 83: 262– 7. 10.1159/000369901 25677445 · DOI · Paper page
  19. [26]Speiser PW Dupont J Zhu D Serrat J Buegeleisen M Tusie-Luna MT. Disease expression and molecular genotype in congenital adrenal hyperplasia due to 21-hydroxylase deficiency. J Clin Invest. (1992) 90: 584– 95. 10.1172/JCI115897 1644925 PMC443137 · DOI · Paper page
  20. [27]Temeck JW Pang SY Nelson C New MI. Genetic defects of steroidogenesis in premature pubarche. J Clin Endocrinol Metab. (1987) 64: 609– 17. 10.1210/jcem-64-3-609 3029158 · DOI
  21. [28]Voutilainen R Jääskeläinen J. Premature adrenarche: etiology, clinical findings, and consequences. J Steroid Biochem Mol Biol. (2015) 145: 226– 36. 10.1016/j.jsbmb.2014.06.004 24923732 · DOI
  22. [29]Oberfield SE Sopher AB Gerken AT. Approach to the girl with early onset of pubic hair. J Clin Endocrinol Metab. (2011) 96: 1610– 22. 10.1210/jc.2011-0225 21602454 PMC3100750 · DOI
  23. [30]Janus D Wojcik M Malunowicz E Starzyk JB. A case of recurrent labial adhesions in a 15-month-old child with asymptomatic non-classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency. J Pediatr Endocrinol Metab. (2012) 25: 1017– 21. 10.1515/jpem-2012-0190 23426836 · DOI
  24. [31]Gopal-Kothandapani JS Petkar A O'Shea E Banerjee I. Perianal hair as an unusual presentation of non-classical congenital adrenal hyperplasia. BMJ Case Rep. (2013) 2013: bcr2013010123. 10.1136/bcr-2013-010123 23814008 PMC3702925 · DOI
  25. [32]Falhammar H Nordenström A. Nonclassic congenital adrenal hyperplasia due to 21-hydroxylase deficiency: clinical presentation, diagnosis, treatment, and outcome. Endocrine. (2015) 50: 32– 50. 10.1007/s12020-015-0656-0 26082286 · DOI · Paper page
  26. [34]Witchel SF. Non-classic congenital adrenal hyperplasia. Steroids. (2013) 78: 747– 50. 10.1016/j.steroids.2013.04.010 23632099 · DOI · Paper page
  27. [35]Carmina E Rosato F Jannì A Rizzo M Longo RA. Extensive clinical experience: relative prevalence of different androgen excess disorders in 950 women referred because of clinical hyperandrogenism. J Clin Endocrinol Metab. (2006) 91: 2– 6. 10.1210/jc.2005-1457 16263820 · DOI · Paper page
  28. [37]Levin JH Carmina E Lobo RA. Is the inappropriate gonadotropin secretion of patients with polycystic ovary syndrome similar to that of patients with adult-onset congenital adrenal hyperplasia? Fertil Steril. (1991) 56: 635– 40. 10.1016/S0015-0282(16)54592-0 1915936 · DOI
  29. [38]Carmina E Lobo RA. Ovarian suppression reduces clinical and endocrine expression of late-onset congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Fertil Steril. (1994) 62: 738– 43. 10.1016/S0015-0282(16)56998-2 7926082 · DOI
  30. [39]Ludwig E. Classification of the types of androgenetic alopecia (common baldness) occurring in the female sex. Br J Dermatol. (1977) 97: 247– 54. 10.1111/j.1365-2133.1977.tb15179.x 921894 · DOI
  31. [40]Trakakis E Papadavid E Dalamaga M Koumaki D Stavrianeas N Rigopoulos D. Prevalence of non-classical congenital adrenal hyperplasia due to 21-hydroxylase deficiency in Greek women with acne: a hospital-based cross-sectional study. J Eur Acad Dermatol Venereol. (2013) 27: 1448– 51. 10.1111/j.1468-3083.2012.04613.x 22703023 · DOI
  32. [41]Arlt W Willis DS Wild SH Krone N Doherty EJ Hahner S. Health status of adults with congenital adrenal hyperplasia: a cohort study of 203 patients. J Clin Endocrinol Metab. (2010) 95: 5110– 21. 10.1210/jc.2010-0917 20719839 PMC3066446 · DOI · Paper page
  33. [42]Saygili F Oge A Yilmaz C. Hyperinsulinemia and insulin insensitivity in women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency: the relationship between serum leptin levels and chronic hyperinsulinemia. Horm Res. (2005) 63: 270– 4. 10.1159/000086363 15956788 · DOI
  34. [44]Han TS Stimson RH Rees DA Krone N Willis DS Conway GS. Glucocorticoid treatment regimen and health outcomes in adults with congenital adrenal hyperplasia. Clin Endocrinol. (2013) 78: 197– 203. 10.1111/cen.12045 22998134 · DOI · Paper page
  35. [45]Van Staa TP Leufkens HG Abenhaim L Zhang B Cooper C. Use of oral corticosteroids and risk of fractures. J Bone Miner Res. (2000) 15: 993– 1000. 10.1359/jbmr.2000.15.6.993 10841167 · DOI · Paper page
  36. [46]Nebesio TD Renbarger JL Nabhan ZM Ross SE Slaven JE Li L. Differential effects of hydrocortisone, prednisone, and dexamethasone on hormonal and pharmacokinetic profiles: a pilot study in children with congenital adrenal hyperplasia. Int J Pediatr Endocrinol. (2016) 2016: 17. 10.1186/s13633-016-0035-5 27688786 PMC5036261 · DOI
  37. [47]Weintrob N Dickerman Z Sprecher E Galatzer A Pertzelan A. Non-classical 21-hydroxylase deficiency in infancy and childhood: the effect of time of initiation of therapy on puberty and final height. Eur J Endocrinol. (1997) 136: 188– 95. 10.1530/eje.0.1360188 9116914 · DOI · Paper page
  38. [49]Dörr HG. Growth in patients with classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Horm Res. (2007) 68(Suppl 5): 93– 9. 10.1159/000110587 18174719 · DOI
  39. [50]Hoepffner W Kaufhold A Willgerodt H Keller E. Patients with classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency can achieve their target height: the Leipzig experience. Horm Res. (2008) 70: 42– 50. 10.1159/000129677 18493149 · DOI
  40. [51]van der Kaay D van den Akker E Ultralow-dose dexamethasone to preserve endogenous cortisol stress response in nonclassical congenital adrenal hyperplasia: a new promising treatment. Int J Endocrinol Metab. (2014) 12: e14657 10.5812/ijem.14657 25237318 PMC4166204 · DOI
  41. [53]McCann-Crosby B Chen M-J Lyons SK Lin Y Axelrad M Dietrich JE. Nonclassical congenital adrenal hyperplasia: targets of treatment and transition. Pediatr Endocrinol Rev. (2014) 12: 224– 38. 25581988
  42. [54]Ogilvie CM Crouch NS Rumsby G Creighton SM Liao L-M Conway GS. Congenital adrenal hyperplasia in adults: a review of medical, surgical and psychological issues. Clin Endocrinol. (2006) 64: 2– 11. 10.1111/j.1365-2265.2005.02410.x 16402922 · DOI
  43. [56]Diaz A Laufer MR Breech LLAA of PC on A, Care AC of O and GC on AH. Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Pediatrics. (2006) 118: 2245– 50. 10.1542/peds.2006-2481 17079600 · DOI · Paper page
  44. [60]Speiser PW Arlt W Auchus RJ Baskin LS Conway GS Merke DP. Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. (2018) 103: 4043– 88. 10.1210/jc.2018-01865 30272171 PMC6456929 · DOI · Paper page
  45. [61]Kruse B Riepe FG Krone N Bosinski HAG Kloehn S Partsch CJ. Congenital adrenal hyperplasia - how to improve the transition from adolescence to adult life. Exp Clin Endocrinol Diabetes. (2004) 112: 343– 55. 10.1055/s-2004-821013 15239019 · DOI
  46. [62]Gastaud F Bouvattier C Duranteau L Brauner R Thibaud E Kutten F. Impaired sexual and reproductive outcomes in women with classical forms of congenital adrenal hyperplasia. J Clin Endocrinol Metab. (2007) 92: 1391– 6. 10.1210/jc.2006-1757 17284631 · DOI
  47. [64]Bidet M Bellanné-Chantelot C Galand-Portier MB Golmard JL Tardy V Morel Y. Fertility in women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency. J Clin Endocrinol Metab. (2010) 95: 1182– 90. 10.1210/jc.2009-1383 20080854 · DOI · Paper page
  48. [65]Birnbaum MD Rose LI. Late onset adrenocortical hydroxylase deficiencies associated with menstrual dysfunction. Obstet Gynecol. (1984) 63: 445– 51. 6322077
  49. [66]Cuhaci N Aydin C Yesilyurt A Pinarli FA Ersoy R Cakir B. Nonclassical congenital adrenal hyperplasia and pregnancy. Case Rep Endocrinol. (2015) 2015: 296924. 10.1155/2015/296924 26558116 PMC4618115 · DOI
  50. [67]Deneux C Tardy V Anne D Mornet E Billaud L Charron D. Phenotype-genotype correlation in 56 women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency. J Clin Endocrinol Metab. (2001) 86: 207– 13. 10.1210/jcem.86.1.7131 11232002 · DOI · Paper page
  51. [68]Simonetti L Bruque CD Fernández CS Benavides-Mori B Delea M Kolomenski JE. CYP21A2 mutation update: Comprehensive analysis of databases and published genetic variants. Hum Mutat. (2018) 39: 5– 22. 10.1002/humu.23351 29035424 · DOI · Paper page
  52. [70]Miller WL Witchel SF. Prenatal treatment of congenital adrenal hyperplasia: risks outweigh benefits. Am J Obstet Gynecol. (2013) 208: 354– 9. 10.1016/j.ajog.2012.10.885 23123167 · DOI · Paper page
  53. [71]Lekarev O New MI. Adrenal disease in pregnancy. Best Pract Res Clin Endocrinol Metab. (2011) 25: 959– 73. 10.1016/j.beem.2011.08.004 22115169 · DOI
  54. [72]New MI Abraham M Yuen T Lekarev O. An update on prenatal diagnosis and treatment of congenital adrenal hyperplasia. Semin Reprod Med. (2012) 30: 396– 9. 10.1055/s-0032-1324723 23044876 · DOI · Paper page
  55. [73]Kazmi D Bailey J Yau M Abu-Amer W Kumar A Low M. New developments in prenatal diagnosis of congenital adrenal hyperplasia. J Steroid Biochem Mol Biol. (2017) 165: 121– 3. 10.1016/j.jsbmb.2016.06.016 27378492 · DOI
  56. [74]Clayton PE Miller WL Oberfield SE Ritzén EM Sippell WG Speiser PW. Consensus statement on 21-hydroxylase deficiency from the European Society for Paediatric Endocrinology and the lawson wilkins pediatric endocrine society. Horm Res. (2002) 58: 188– 95. 10.1159/000065490 12324718 · DOI
  57. [75]Nandagopal R Sinaii N Avila NA Van Ryzin C Chen W Finkielstain GP. Phenotypic profiling of parents with cryptic nonclassic congenital adrenal hyperplasia: findings in 145 unrelated families. Eur J Endocrinol. (2011) 164: 977– 84. 10.1530/EJE-11-0019 21444649 PMC3470911 · DOI · Paper page
  58. [76]Takasu N Nakachi K Higa H. Development of Graves' hyperthyroidism caused an adrenal crisis in a patient with previously unrecognized non-classical 21-hydroxylase deficiency. Intern Med. (2010) 49: 1395– 400. 10.2169/internalmedicine.49.3573 20647655 · DOI
  59. [77]Meyer-Bahlburg HFL Dolezal C Baker SW Carlson AD Obeid JS New MI Prenatal androgenization affects gender-related behavior but not gender identity in 5-12-year-old girls with congenital adrenal hyperplasia. Arch Sex Behav. (2004) 33: 97– 104. 10.1023/B:ASEB.0000014324.25718.51 15146142 · DOI
  60. [78]Meyer-Bahlburg HFL Dolezal C Baker SW New MI. Sexual orientation in women with classical or non-classical congenital adrenal hyperplasia as a function of degree of prenatal androgen excess. Arch Sex Behav. (2008) 37: 85– 99. 10.1007/s10508-007-9265-1 18157628 · DOI · Paper page

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Authors
Livadas, S., & Bothou, C.
Affiliations
  • Metropolitan Hospital (GR)
  • University Hospital Zurich (CH)
Corresponding author
Livadas, Sarantis
Venue
Frontiers in Endocrinology
Published
2019-06-06
Volume
10
Pages
366-366
ISSN
1664-2392 (ISSN-L)
OpenAlex
W2966291464
Cited by
57
References
17
Citations by year
2026: 6 · 2025: 5 · 2024: 6 · 2023: 14 · 2022: 8 · 2021: 12 · 2020: 6
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0.57
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Endocrinology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
  • Zurich Open Repository and Archive (University of Zurich)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
Keywords
non-classical congenital adrenal hyperplasia, female patients, hyperandrogenism, premature pubarche, dexamethasone, menstrual cycle restoration, hirsutism, acne, subfertility, fertility, oral contraceptives, androgen receptor antagonists, genotype-phenotype variability, ACTH stimulation test, molecular diagnosis, pregnancy management

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