LETTER TO EDITOR
Year : 2011 | Volume
: 4 | Issue : 2 | Page : 101--102
Finasteride and male fertility
Department of Internal Medicine, Medwin Hospital, Nampally, Hyderabad, Andhra Pradesh, India
Department of Internal Medicine, AMC, 3rd Floor, Medwin Hospital, Chirag Ali lane, Nampally, Hyderabad - 500 001, Andhra Pradesh
|How to cite this article:|
Gude D. Finasteride and male fertility.J Hum Reprod Sci 2011;4:101-102
|How to cite this URL:|
Gude D. Finasteride and male fertility. J Hum Reprod Sci [serial online] 2011 [cited 2013 May 23 ];4:101-102
Available from: http://www.jhrsonline.org/text.asp?2011/4/2/101/86093
Finasteride is a specific and competitive inhibitor of 5-α-reductase enzyme Type 2, inhibiting the conversion of testosterone to dihydrotestosterone (DHT). It has been approved for treatment of benign prostatic hyperplasia and male pattern baldness, resulting in widespread use in men in reproductive age. There are reports concerning fertility in those taking the drug and I attempt to review the literature on the same.
In a study, a 48-year-old man on finasteride found a decrease in his sperm DNA fragmentation index (DFI) by 9% three months after discontinuing the drug and a further fall of about 5% in the subsequent three months.  Similar improvement was observed in two other cases of azoospermia and severe oligospermia, 6 months after discontinuing finasteride. 
A patient on finasteride (1 mg) for 1 year, diagnosed with oligospermia (impaired spermatogenesis) 5 years earlier, was found to have increased semen volume immediately after cessation of finasteride and his sperm concentration improved to more than 10 × 10 6 /ml about 4 months later. 
In a randomized, double-blinded, placebo-controlled trial of 99 men (age, 18-55 years; 33 of them assigned to receive 0.5 mg dutasteride, 34 receiving 5 mg finasteride, and the remaining on placebo) for 1 year, the serum prostate-specific antigen (PSA) and self-assessed sexual function (measured per validated questionnaire) decreased during treatment with both 5-a-reductase inhibitors (but returned to baseline during follow-up).  Except sperm morphology, all semen parameters are known to be compromised by finasteride. Another observation showed similar findings of decreased semen parameters, which were reversible.
In experimental models, finasteride in vitro caused a significant reduction in the number of spermatogenic cells, diameter of seminiferous tubules, and diameter and thickness of epididymis tubules, although the effects were not seen in vivo. However, in both in vitro and in vivo, the diameter of prostatic tubules decreased significantly. 
The effects of finasteride in the female counterparts of men on the drug were analyzed in two studies. While the first study calculated the amount of finasteride in the pregnant women to be 50- to 100-fold less than the least possible dose that could affect circulating DHT levels in men, the second study derived that finasteride levels were about 750 times lower than the 'no effect' level that resulted in developmental abnormalities in rhesus monkeys.  Hence, it is safe to assume that there is negligible risk to the partners. But direct finasteride administration in pregnant women is reported to cause abnormalities to the genitalia of the male fetus.
A study reported that spermatogenesis is not adversely affected by finasteride (at 1 mg dose), although the same study observed that the ejaculate volume, prostate volume, and serum PSA showed a decrease with finasteride administration. 
Finasteride does not have negative effects on erectile function, as established by many studies using international index of erectile function-5 questionnaire and nocturnal penile tumescence testing.
Although the effects of finasteride on male fertility needs further extensive testing, caution (examining sperm DFI, a trial of discontinuation, etc) is warranted for its administration, especially in infertile men.
The author thanks colleagues and staff of Internal Medicine Department, Medwin Hospital, India.
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