A man wrote to me about this problem with his baby who developed a problem unique to 5 alpha reductase inhibitors
This is what Merck wrote:
Although the above comments reference 2 studies using a 5?mg dose, Merck (2007) also measured semen levels of finasteride in patients taking a 1?mg dose. The men were treated with 1 mg for 6 weeks. The highest level measured was 1.52 ng/mL, and the mean level was 0.26 ng/mL. Using the highest measured level (1.52 ng/mL), women exposed to a 5?mL ejaculate per day would be exposed to 7.6 ng/d (assuming 100% vaginal absorption). Merck (2007) found this level to be 750 times lower than the “no effect” level for developmental abnormalities in rhesus monkeys.
In summary, a 1?mg dose of finasteride does not appear to adversely affect spermatogenesis. In addition, the level present in the ejaculate of patients taking 1 mg appears to be negligible. Thus, there does not appear to be any need to stop 1 mg of finasteride in those patients trying to conceive or in those whose partners are pregnant.
This is what is really the issue:
Mohan et al states which clearly shows that even a small amount of finasteride that comes through the semen, the risk is real:
“Congenital scrotal agenesis is a rare anomaly that, to our knowledge, has only been reported in the literature on four previous occasions.. Scrotal development is initiated in the 7th embryonic week with the formation of labioscrotal folds on either side of the urogenital folds. Foetal testosterone is converted into more potent dihydro-testosterone by the action of the enzyme 5a-reductase type 2 which is expressed in these tissues. The scrotum is then formed as a result of enlargement and midline fusion of the labio-scrotal folds in response to the androgens…
Sinnecker et al. have shown that that 5a-reductase type 2 deficiency can result in a spectrum of phenotypes with varying degrees of virilization spanning from completely female to almost normal male. The phenotypes reported in our cases could be explained by a localised deficiency of 5a-reductase type 2, limited to the labioscrotal folds. This could possibly result in partial virilization of labioscrotal folds where in there is absence of development of normal scrotum but at the same time labioscrotal folds are prevented from developing into the complete female phenotype, i.e. labia majora. Later during topical therapy, the incompletely virilized labio- scrotal folds could have developed into normal scrotal tissue under the influence high concentration of testosterone. This is akin to the development of normal male external genitalia in children with 5a-reductase type 2 deficiency during pubertal testosterone surge.”
This condition is directly linked to 5a-reductase type 2 deficiency. I will get him all of the best medical treatment possible but I don’t believe the guilt will ever leave me. This is still a happy time with a baby but also the most traumatic. Thank you for your offer, I appreciate it. Please publicise these risks as much as possible as well. I look forward to hearing from you more in future.
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