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Post-finasteride syndrome: a surmountable challenge for clinicians
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<blockquote data-quote="madman" data-source="post: 171444" data-attributes="member: 13851"><p>[ATTACH=full]9201[/ATTACH]</p><p><strong><span style="color: rgb(184, 49, 47)">(A)</span> A hypothetical model of finasteride acting as an endocrine disruptor. Finasteride via inhibiting key neuro-steroid biosynthesis promotes epigenetic changes in gene expression leading to silencing or attenuating physiological responses. Inhibition of 5a-reductases activities by the high affinity, slow dissociating inhibitor <span style="color: rgb(184, 49, 47)">(finasteride)</span> results in depleting the substrate precursors for the 3a-hydroxy-steroid dehydrogenases and therefore blocking biosynthesis of neuro-steroids. This inhibition results in attenuating the function of neurotransmitter receptors and promotes changes in the expression of a host of gene products, thus eliciting epigenetic changes manifested in histone acetylation, methylation, and DNA methylation and upregulation of androgen receptor <span style="color: rgb(184, 49, 47)">(AR)</span> gene expression. These changes together with depleted neurosteroid pool manifest itself in the development of PFS in susceptible individuals. <span style="color: rgb(184, 49, 47)">(B) </span>The epigenetic changes induced by finasteride elicited endocrine disruption, illustrated in a, produce pathophysiological changes that are manifested as constellations of symptoms of PFS. <span style="color: rgb(184, 49, 47)">(Adapted, with permission from the publisher, from Traish AM. The post-finasteride syndrome: clinical manifestation of drug-induced epigenetics due to endocrine disruption. Current Sexual Health Reports 2018;10(3):88–103.) </span></strong></p></blockquote><p></p>
[QUOTE="madman, post: 171444, member: 13851"] [ATTACH=full]9201[/ATTACH] [B][COLOR=rgb(184, 49, 47)](A)[/COLOR] A hypothetical model of finasteride acting as an endocrine disruptor. Finasteride via inhibiting key neuro-steroid biosynthesis promotes epigenetic changes in gene expression leading to silencing or attenuating physiological responses. Inhibition of 5a-reductases activities by the high affinity, slow dissociating inhibitor [COLOR=rgb(184, 49, 47)](finasteride)[/COLOR] results in depleting the substrate precursors for the 3a-hydroxy-steroid dehydrogenases and therefore blocking biosynthesis of neuro-steroids. This inhibition results in attenuating the function of neurotransmitter receptors and promotes changes in the expression of a host of gene products, thus eliciting epigenetic changes manifested in histone acetylation, methylation, and DNA methylation and upregulation of androgen receptor [COLOR=rgb(184, 49, 47)](AR)[/COLOR] gene expression. These changes together with depleted neurosteroid pool manifest itself in the development of PFS in susceptible individuals. [COLOR=rgb(184, 49, 47)](B) [/COLOR]The epigenetic changes induced by finasteride elicited endocrine disruption, illustrated in a, produce pathophysiological changes that are manifested as constellations of symptoms of PFS. [COLOR=rgb(184, 49, 47)](Adapted, with permission from the publisher, from Traish AM. The post-finasteride syndrome: clinical manifestation of drug-induced epigenetics due to endocrine disruption. Current Sexual Health Reports 2018;10(3):88–103.) [/COLOR][/B] [/QUOTE]
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Post-finasteride syndrome: a surmountable challenge for clinicians
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