21-hydroxylase deficiency classification: Difference between revisions
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{{21-hydroxylase deficiency}} | {{21-hydroxylase deficiency}} | ||
{{CMG}}; '''Associate Editor-In-Chief:''' {{MJ}} | {{CMG}}; '''Associate Editor-In-Chief:''' {{MJ}}, {{AAM}} | ||
==Overview== | ==Overview== | ||
21-hydroxylase deficiency may be classified | 21-hydroxylase deficiency may be classified according to the severity of disease and time of onset into two forms, classic and non-classic. The classic form can be sub-divided into two sub-types, which are salt-wasting and non-salt wasting 21-hydroxylase deficiency. | ||
== | ==Classification== | ||
21- | 21-hydroxylase deficiency my be classified by clinical manifestations in to two forms: | ||
*Classical form, most severe form of 21-hydroxylase deficiency, presents during the neonatal period and early infancy. The | *Classical form, most severe form of 21-hydroxylase deficiency, presents during the [[neonatal]] period and early [[infancy]]. The classic form can be classified in to two subtypes based on [[aldosterone]] status: | ||
** | **Classic salt wasting, [[aldosterone]] deficient. | ||
** | **Classic non-salt wasting, normal [[aldosterone]]. | ||
*Non- | *Non-classic form or late-onset 21-hydroxylase deficiency, presents later during the [[adolescence]] period.<ref name="pmid10857554">{{cite journal |vauthors=White PC, Speiser PW |title=Congenital adrenal hyperplasia due to 21-hydroxylase deficiency |journal=Endocr. Rev. |volume=21 |issue=3 |pages=245–91 |year=2000 |pmid=10857554 |doi=10.1210/edrv.21.3.0398 |url=}}</ref><ref name="pmid20823466">{{cite journal |vauthors=Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC |title=Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline |journal=J. Clin. Endocrinol. Metab. |volume=95 |issue=9 |pages=4133–60 |year=2010 |pmid=20823466 |pmc=2936060 |doi=10.1210/jc.2009-2631 |url=}}</ref> | ||
== References == | == References == | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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{{WH}} | |||
[[Category:Disease]] | |||
[[Category:Pediatrics]] | |||
[[Category:Endocrinology]] | |||
[[Category:Genetic disorders]] | |||
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Latest revision as of 15:40, 24 July 2020
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21-hydroxylase deficiency Microchapters |
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Differentiating 21-Hydroxylase Deficiency from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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21-hydroxylase deficiency classification On the Web |
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American Roentgen Ray Society Images of 21-hydroxylase deficiency classification |
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Risk calculators and risk factors for 21-hydroxylase deficiency classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Mehrian Jafarizade, M.D [2], Ahmad Al Maradni, M.D. [3]
Overview
21-hydroxylase deficiency may be classified according to the severity of disease and time of onset into two forms, classic and non-classic. The classic form can be sub-divided into two sub-types, which are salt-wasting and non-salt wasting 21-hydroxylase deficiency.
Classification
21-hydroxylase deficiency my be classified by clinical manifestations in to two forms:
- Classical form, most severe form of 21-hydroxylase deficiency, presents during the neonatal period and early infancy. The classic form can be classified in to two subtypes based on aldosterone status:
- Classic salt wasting, aldosterone deficient.
- Classic non-salt wasting, normal aldosterone.
- Non-classic form or late-onset 21-hydroxylase deficiency, presents later during the adolescence period.[1][2]
References
- ↑ White PC, Speiser PW (2000). "Congenital adrenal hyperplasia due to 21-hydroxylase deficiency". Endocr. Rev. 21 (3): 245–91. doi:10.1210/edrv.21.3.0398. PMID 10857554.
- ↑ Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC (2010). "Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 95 (9): 4133–60. doi:10.1210/jc.2009-2631. PMC 2936060. PMID 20823466.