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The cause was determined to be 5α-Reductase deficiency, and the results were published in the journal Science in 1974. The frequency of the deficiency was found to be unusually high in Las Salinas, with occurrence ratio of 1 güevedoce to every 90 unaffected males. [11]
5α-Reductase 2 deficiency (5αR2D) is an autosomal recessive condition caused by a mutation in SRD5A2, a gene encoding the enzyme 5α-reductase type 2 (5αR2). People with this condition are genetically male, with one X and one Y chromosome in each cell, and they have testes .
5α-Reductase type 1 inactivated male mice have reduced bone mass and forelimb muscle grip strength, which has been proposed to be due to lack of 5α-reductase type 1 expression in bone and muscle. [29] In 5 alpha reductase type 2 deficient males, the type 1 isoenzyme is thought to be responsible for their virilization at puberty. [6]
[5] [100] [101] The clinical relevance of the results published by Auchus in 2004 was demonstrated in 2012 for the first time when Kamrath et al. [17] attributed the urinary metabolites to the androgen backdoor pathway from 17OHP to DHT in patients with steroid 21-hydroxylase (encoded by the gene CYP21A2) enzyme deficiency. [102] [103] [104] [5]
The human gene SRD5A2 encodes the 3-oxo-5α-steroid 4-dehydrogenase 2 enzyme, also known as 5α-reductase type 2 (5αR2), [5] [6] one of three isozymes of 5α-reductase.. 5αR2 catalyzes the conversion of the male sex hormone testosterone into the more potent androgen, dihydrotestosterone.
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