11β-hydroxylase deficiency risk factors: Difference between revisions
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The most potent risk factor in the development of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency is presence of [[family history]] of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency.<ref name="pmid28476231">{{cite journal |vauthors=Hannah-Shmouni F, Chen W, Merke DP |title=Genetics of Congenital Adrenal Hyperplasia |journal=Endocrinol. Metab. Clin. North Am. |volume=46 |issue=2 |pages=435–458 |year=2017 |pmid=28476231 |doi=10.1016/j.ecl.2017.01.008 |url=}}</ref> | The most potent risk factor in the development of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency is presence of [[family history]] of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency.<ref name="pmid28476231">{{cite journal |vauthors=Hannah-Shmouni F, Chen W, Merke DP |title=Genetics of Congenital Adrenal Hyperplasia |journal=Endocrinol. Metab. Clin. North Am. |volume=46 |issue=2 |pages=435–458 |year=2017 |pmid=28476231 |doi=10.1016/j.ecl.2017.01.008 |url=}}</ref> | ||
==References== | ==References== | ||
{{Reflist| | {{Reflist|2}} | ||
[[Category:Disease]] | [[Category:Disease]] | ||
Revision as of 20:37, 19 July 2017
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11β-hydroxylase deficiency Microchapters |
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Differentiating 11β-hydroxylase deficiency from other Diseases |
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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 congenital adrenal hyperplasia due to 11β-hydroxylase deficiency is the presence of family history of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency.
Risk Factors
The most potent risk factor in the development of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency is presence of family history of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency.[1]
References
- ↑ Hannah-Shmouni F, Chen W, Merke DP (2017). "Genetics of Congenital Adrenal Hyperplasia". Endocrinol. Metab. Clin. North Am. 46 (2): 435–458. doi:10.1016/j.ecl.2017.01.008. PMID 28476231.