21-hydroxylase deficiency risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The most potent [[risk factor]] in the development of 21-hydroxylase deficiency is presence of [[family history]] of 21-hydroxylase deficiency, and belonging to certain [[Ethnic group|ethnic groups]], particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits. | The most potent [[risk factor]] in the development of [[21-hydroxylase]] deficiency is presence of [[family history]] of 21-hydroxylase deficiency, and belonging to certain [[Ethnic group|ethnic groups]], particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits. | ||
==Risk Factors== | ==Risk Factors== | ||
The most potent risk factors in the development of 21-hydroxylase deficiency are: | The most potent risk factors in the development of 21-hydroxylase deficiency are: | ||
* Presence of [[family history]] of 21-hydroxylase deficiency. | * Presence of [[family history]] of [[21-hydroxylase]] deficiency. | ||
* Belonging to certain ethnic groups, particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits.<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><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> | * Belonging to certain ethnic groups, particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits.<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><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> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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Latest revision as of 15:37, 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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21-hydroxylase deficiency risk factors On the Web |
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Risk calculators and risk factors for 21-hydroxylase deficiency risk factors |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]
Overview
The most potent risk factor in the development of 21-hydroxylase deficiency is presence of family history of 21-hydroxylase deficiency, and belonging to certain ethnic groups, particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits.
Risk Factors
The most potent risk factors in the development of 21-hydroxylase deficiency are:
- Presence of family history of 21-hydroxylase deficiency.
- Belonging to certain ethnic groups, particularly Ashkenazi Jews, Yugoslavians and Yupik Inuits.[1][2]
References
- ↑ 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.
- ↑ 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.