17-beta-hydroxysteroid dehydrogenase deficiency pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | |||
17-beta-hydroxysteroid dehydrogenase deficiency-3 is biochemically characterized by decreased levels of testosterone and increased levels of androstenedione as a result of the defect in conversion of androstenedione into testosterone. This leads to clinically important higher ratio of androstenedione to testosterone (A'dion/T) (see figure). | |||
[[Image:Test biosynth 17BHSD3.jpg|thumb|center|600px| Biochemical effects of 17β-hydroxysteroid deficiency-3 in testosterone biosynthesis. Typically levels of androstenedione are significantly increased, whilst testosterone levels are decreased, leading to male [[undervirilization]].]] | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 14:41, 19 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
17-beta-hydroxysteroid dehydrogenase deficiency-3 is biochemically characterized by decreased levels of testosterone and increased levels of androstenedione as a result of the defect in conversion of androstenedione into testosterone. This leads to clinically important higher ratio of androstenedione to testosterone (A'dion/T) (see figure).
