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Androstenedione is created from dehydroepiandrosterone (DHEA) or 17-hydroxyprogesterone. [ 10 ] A deficiency in the HSD17B3 gene is characterized biochemically by decreased levels of testosterone which results in the insufficient formation of dihydrotestosterone during fetal development.
Additional treatments to optimize growth by delaying puberty or delaying bone maturation [citation needed] If CAH is caused by the deficiency of the 21-hydroxylase enzyme, then treatment aims to normalize levels of androstenedione, but normalization of 17α-hydroxyprogesterone is a sign of overtreatment. [32]
The exact cause for the varied collection of symptoms found in the different ALD phenotypes is not clear. The white matter of the brain, the Leydig cells of the testes and the adrenal cortex are the most severely affected systems. [1] The excess VLCFA can be detected in almost all tissues of the body, despite the localization of symptoms. [1]
Serum levels of 17OHP, testosterone, androstenedione, and other adrenal steroids are followed for additional information, but may not be entirely normalized even with optimal treatment. As regular monitoring is needed, patients can be monitored non-invasively by measuring 17OHP and androstenedione in saliva. [ 211 ] (
Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene CYP17A1, which produces the enzyme 17α-hydroxylase. [1] [2] It causes decreased synthesis of cortisol and sex hormones, with resulting increase in mineralocorticoid production.
Adrenal steroids such as glucocorticoids and mineralocorticoids are commonly used as treatments in diseases such as Congenital adrenal hyperplasia. [2] CAH commonly causes overproduction of androgens, glucocorticoid treatment is used to reduce Adrenocorticotropic hormone (ACTH) and reduce the production of androgens allowing for symptoms of CAH to be managed though treatment is required to be ...