Abstract:Herein, we present an unusual case of secondary infertility after prolonged use of low-dose finasteride for androgenetic alopecia in a 40-year-old man. We detected sperm DNA damage in the patient. Despite such a long-term use, we observed that impairment in semen parameters and sperm DNA fragmentation index regressed after the drug was discontinued. Consequently, pregnancy occurred and resulted in live birth.
“…Although in our study, we did not perform any analysis of the spermatozoa genome, the difficulties in obtaining pups from female rats fertilized by finasteride-treated male rats could be associated with molecular abnormalities in the sperm, as shown in other studies [22][23][24]. Firstly, we observed the low number of pups in the litters.…”
Section: Discussionmentioning
confidence: 69%
“…Moreover, female pups predominated in many litters in our experiment. As was mentioned above, even a low dose of finasteride might exert a negative effect on sperm DNA integrity [22][23][24]; thus, the unequal distribution of sexes in the litters may have been caused by some genetic changes in the spermatozoa chromosomes of the finasteride-treated rats. Possibly, finasteride like endocrine disruptors could induce transgenerational effect.…”
Section: Discussionmentioning
confidence: 93%
“…Caution has been also advised regarding the use of finasteride by male members of couples who plan to have children [44]. Finasteride-induced secondary infertility is speculated to be correlated with higher sperm DNA fragmentation indices [22,23], 1818XY diploidy, and 19XY disomy [24]. Approximately 95% of the length of the human Y chromosome is taken up by a nonrecombining region (NRY) that contains the majority (50-60%) of the encoding genes inherited from father to son.…”
Section: Discussionmentioning
confidence: 99%
“…In spite of these persistent sexual side effects, patients also suffer from melancholy, depressive syndromes, and suicidal thoughts [21]. Other case reports reveal that low-dose finasteride results in sperm DNA damage (elevated sperm DNA fragmentation index) [22,23]. Transmission electron microscopy studies revealed altered sperm morphology consistent with necrosis, and FISH data showed elevated frequencies of diploidy and sex chromosome disomy [24].…”
Introduction. The hormone-dependent events that occur throughout the first wave of spermatogenesis, such as the establishment of the number of Sertoli cells (SCs) and spermatogonial stem cells (SSCs) within the seminiferous cords and the setting up of the blood-testis barrier, are important for adult male fertility. Any changes in the T/DHT ratio can result in male subfertility or even infertility. In this study we aimed to evaluate effects of paternal exposure to 5-alpha reductase type 2 inhibitor, finasteride on litter size, androgen levels and germ cell apoptosis in male offspring during postnatal development. Material and methods. The subjects of the study were 7, 14, 21/22, 28, and 90-day-old Wistar male rats (F1:Fin) born from females fertilized by finasteride-treated rats. Offspring born from untreated parental animals were used as a control group (F1:Control). Animals and the collected testes were weighed, blood and intratesticular levels of T and DHT were measured by ELISA, and the apoptotic index of testicular cells was evaluated by TUNEL technique. Results. We observed difficulties in obtaining male newborns from female rats fertilized by finasteride-treated male rats. In the F1:Fin rats, changes in the body and testes weights occurred, and a lower number of apoptotic cells was found during postnatal maturation of the seminiferous epithelium. Changes in androgen concentrations during the first spermatogenesis wave and adult life were also evident. Conclusion. Finasteride treatment of male adult rats may not only cause a decrease in the fertility of parental rats, but also could lead to incorrect, androgen-sensitive course of spermatogenesis in their offspring.
“…Although in our study, we did not perform any analysis of the spermatozoa genome, the difficulties in obtaining pups from female rats fertilized by finasteride-treated male rats could be associated with molecular abnormalities in the sperm, as shown in other studies [22][23][24]. Firstly, we observed the low number of pups in the litters.…”
Section: Discussionmentioning
confidence: 69%
“…Moreover, female pups predominated in many litters in our experiment. As was mentioned above, even a low dose of finasteride might exert a negative effect on sperm DNA integrity [22][23][24]; thus, the unequal distribution of sexes in the litters may have been caused by some genetic changes in the spermatozoa chromosomes of the finasteride-treated rats. Possibly, finasteride like endocrine disruptors could induce transgenerational effect.…”
Section: Discussionmentioning
confidence: 93%
“…Caution has been also advised regarding the use of finasteride by male members of couples who plan to have children [44]. Finasteride-induced secondary infertility is speculated to be correlated with higher sperm DNA fragmentation indices [22,23], 1818XY diploidy, and 19XY disomy [24]. Approximately 95% of the length of the human Y chromosome is taken up by a nonrecombining region (NRY) that contains the majority (50-60%) of the encoding genes inherited from father to son.…”
Section: Discussionmentioning
confidence: 99%
“…In spite of these persistent sexual side effects, patients also suffer from melancholy, depressive syndromes, and suicidal thoughts [21]. Other case reports reveal that low-dose finasteride results in sperm DNA damage (elevated sperm DNA fragmentation index) [22,23]. Transmission electron microscopy studies revealed altered sperm morphology consistent with necrosis, and FISH data showed elevated frequencies of diploidy and sex chromosome disomy [24].…”
Introduction. The hormone-dependent events that occur throughout the first wave of spermatogenesis, such as the establishment of the number of Sertoli cells (SCs) and spermatogonial stem cells (SSCs) within the seminiferous cords and the setting up of the blood-testis barrier, are important for adult male fertility. Any changes in the T/DHT ratio can result in male subfertility or even infertility. In this study we aimed to evaluate effects of paternal exposure to 5-alpha reductase type 2 inhibitor, finasteride on litter size, androgen levels and germ cell apoptosis in male offspring during postnatal development. Material and methods. The subjects of the study were 7, 14, 21/22, 28, and 90-day-old Wistar male rats (F1:Fin) born from females fertilized by finasteride-treated rats. Offspring born from untreated parental animals were used as a control group (F1:Control). Animals and the collected testes were weighed, blood and intratesticular levels of T and DHT were measured by ELISA, and the apoptotic index of testicular cells was evaluated by TUNEL technique. Results. We observed difficulties in obtaining male newborns from female rats fertilized by finasteride-treated male rats. In the F1:Fin rats, changes in the body and testes weights occurred, and a lower number of apoptotic cells was found during postnatal maturation of the seminiferous epithelium. Changes in androgen concentrations during the first spermatogenesis wave and adult life were also evident. Conclusion. Finasteride treatment of male adult rats may not only cause a decrease in the fertility of parental rats, but also could lead to incorrect, androgen-sensitive course of spermatogenesis in their offspring.
“…Interestingly, (Şalvarci at al. 2013) reported a case of secondary infertility due to the use of low–dose finasteride, based on DNA integrity which improved after drug cessation [6]. …”
IntroductionOld men preparing themselves for marriage late in their lives might face infertility. Infertility in this group of men should be considered from a wider perspective, as they face any age–related health troubles that include, but are not limited to, androgen deficiency and psychological disorders that impede early conception. This review aims to shed light on the proper approach to this minority of secondarily infertile men.Material and methodsA comprehensive electronic English literature search was conducted, using various medical websites and books, for the factors that cause infertility in senior fathers. The physiology of geriatric males, together with their common comorbidities, were discussed.ResultsOld men presenting with secondary infertility should be approached differently. Aging, itself, has a significant impact on male sexual function, sperm parameters, and fertility; all of which contribute to poor fecundability, decreased fertilizing capacity, increased time to pregnancy, increased rate of DNA damage, high abortion rates and increased prevalence of fetal developmental failures. The complexity and the unknowns of the aging male physiology, together with the interaction of obstinate diseases the patient might have, make the issue very difficult to tackle.ConclusionsManagement should include the conventional way of treating young sufferers and further target the underlying causes, if known, along with the provision of geriatric, psychologic, and andrologic support.
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