I don’t know, I’m not an endocrinologist. Would have to research more, but I believe likely treatment would be androgen replacement (TRT). Something else I came across was this (hypospadia is an undeveloped penis)… but note the pathways involved, some of which are discussed in this thread already:
Defects of the Testosterone Biosynthetic Pathway in Boys With Hypospadias
linkinghub.elsevier.com/retrieve … 4701648936
Purpose
We determined the incidence of defects in 3 enzymes, namely 3 beta-hydroxysteroid dehydrogenase, 17 alpha-hydroxylase and 17,20-lyase, on the testosterone biosynthetic pathway in boys with hypospadias.
Materials and Methods
We evaluated 30 boys with a 46,XY karyotype, fully descended testes and penoscrotal or proximal shaft hypospadias. Serum concentrations of the metabolites mediated by these enzymes were measured, from which the precursor-to-product ratios were calculated. Seven patients underwent adrenocorticotropic hormone stimulation. Findings were compared to previously published data on age matched normal boys.
Results
A total of 11 boys had evidence of impaired function of 3 beta-hydroxysteroid dehydrogenase alone or in combination with impaired 17,20-lyase or 17 alpha-hydroxylase activity. An additional 4 boys had evidence of isolated 17,20-lyase deficiency. Thus, of the 30 boys studied 15 (50%) had evidence of a testosterone biosynthetic defect. The effect of adrenocorticotropic hormone stimulation varied with widening of the precursor-to-product ratios in some boys and narrowing in others.
Conclusions
A high incidence of 3 beta-hydroxysteroid dehydrogenase and 17,20-lyase deficiency was found in boys with proximal hypospadias. The response to adrenocorticotropic hormone stimulation suggests that enzymes in the adrenal glands and testes may be affected independently. Our findings support the hypothesis that hypospadias is the result of fetal endocrinopathy.