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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Dutasteride vs Finasteride
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<blockquote data-quote="madman" data-source="post: 145408" data-attributes="member: 13851"><p>Not only does Dutasteride have a stronger effect on suppressing DHT.....hence a lower dose is needed but it inhibits both Type 1 and 2 (5AR) as opposed to Finasteride which only inhibits Type 2 (5AR).</p><p></p><p></p><p></p><p></p><p><strong>Comparison of Clinical Trials With Finasteride and Dutasteride <span style="color: rgb(184, 49, 47)">(2004)</span></strong></p><p><strong></strong></p><p><strong>Abstract</strong></p><p></p><p><em>Finasteride selectively inhibits the Type 2 isoenzyme of 5α-reductase (5AR) (the enzyme responsible for converting testosterone to dihydrotestosterone [DHT]) <strong>whereas <span style="color: rgb(184, 49, 47)">dutasteride inhibits both Type 1 and Type 2 5AR.</span> </strong>General conclusions regarding the differences and similarities of these 2 agents, in terms of pharmacologic effect, safety, and efficacy, can be drawn from the evaluation of short-term comparative trials and similar but non-comparative long-term trials. <strong><span style="color: rgb(184, 49, 47)">Dutasteride therapy </span>reduces <span style="color: rgb(184, 49, 47)">serum DHT significantly </span>more than finasteride.</strong> In men with benign prostatic hyperplasia (BPH), treatment with either agent results in similar prostate gland volume reduction, flow rate, and symptom improvement, and similar reductions in long-term risk of BPH development in terms of symptom progression and acute urinary retention (AUR) and BPH-related surgery. There does not appear to be any clinically significant difference between the adverse event profiles of dutasteride and finasteride. Although weak evidence suggests a difference in the onset of clinical benefit, the available non-comparative trial data do not confirm this finding. Patients with symptomatic BPH who receive dutasteride or finasteride, either as monotherapy or combination therapy with α-blockers, can expect to experience significant prostate gland size reduction, improved symptoms, and reduced risk of progression in terms of long-term adverse outcomes.</em></p><p></p><p></p><p></p><p></p><p></p><p></p><p></p><p></p><p></p><p><strong>Figure 1</strong></p><p><strong></strong></p><p><strong>The 2 5α-reductase inhibitors (5ARIs), dutasteride and finasteride, suppress dihydrotestosterone (DHT) by inhibiting the conversion of testosterone to DHT. Finasteride inhibits only the Type 2 5AR isoenzyme, whereas <span style="color: rgb(184, 49, 47)">dutasteride, the only dual 5ARI, selectively inhibits both Type 1 and Type 2 5AR isoenzymes.</span> Data from Bartsch G et al.</strong><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/#B1" target="_blank"><strong>1</strong></a></p><p>[ATTACH=full]7271[/ATTACH]</p><p></p><p></p><p><strong>Figure 2</strong></p><p><strong></strong></p><p><strong>A comparative phase II evaluation of dutasteride and finasteride in a double-blind placebo-controlled trial <span style="color: rgb(184, 49, 47)">clearly demonstrates</span> that <span style="color: rgb(184, 49, 47)">serum dihydrotestosterone (DHT) suppression is significantly greater with dutasteride (0.5 mg daily) </span>than with finasteride (5 mg daily). Data from Clark RV et al.</strong><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/#B3" target="_blank"><strong>3</strong></a></p><p>[ATTACH=full]7272[/ATTACH]</p><p></p><p></p><p></p><p></p><p><strong>Conclusion</strong></p><p><strong></strong></p><p><strong><em>Without evidence from <span style="color: rgb(184, 49, 47)">long-term clinical trials comparing the safety and efficacy of dutasteride and finasteride</span>, firm conclusions regarding the relative <span style="color: rgb(184, 49, 47)">efficacy and safety </span>of one agent over the other cannot be made. </em></strong><em><strong><span style="color: rgb(184, 49, 47)">However, indirect comparisons of long-term changes in prostate volume and symptoms (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/figure/F5/" target="_blank">Figures 5A and B</a>) and general conclusions drawn from the evaluation of short-term comparative trials and similar but non-comparative long-term trials can be made (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/table/T4/" target="_blank">Table 4</a>). </span>One such conclusion is that <span style="color: rgb(184, 49, 47)">dutasteride therapy reduces serum DHT significantly more</span> than finasteride. In addition, treatment with either agent results in <span style="color: rgb(184, 49, 47)">similar prostate gland volume reduction, flow rate, and symptom improvement, </span><span style="color: rgb(0, 0, 0)">and</span><span style="color: rgb(184, 49, 47)"> similar reductions in long-term risk of BPH development </span><span style="color: rgb(0, 0, 0)">i</span>n terms of symptom progression and AUR and BPH-related surgery. There does not appear to be any clinically significant difference between the adverse event profile of dutasteride and finasteride. Although weak evidence suggests a difference in the onset of clinical benefit, the available non-comparative trial data do not confirm this finding. Patients with symptomatic BPH who receive dutasteride or finasteride, either as monotherapy or combination therapy with α-blockers, can expect to experience significant prostate gland size reduction, improved symptoms, and reduced risk of progression in terms of long-term adverse outcomes.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 145408, member: 13851"] Not only does Dutasteride have a stronger effect on suppressing DHT.....hence a lower dose is needed but it inhibits both Type 1 and 2 (5AR) as opposed to Finasteride which only inhibits Type 2 (5AR). [B]Comparison of Clinical Trials With Finasteride and Dutasteride [COLOR=rgb(184, 49, 47)](2004)[/COLOR] Abstract[/B] [I]Finasteride selectively inhibits the Type 2 isoenzyme of 5α-reductase (5AR) (the enzyme responsible for converting testosterone to dihydrotestosterone [DHT]) [B]whereas [COLOR=rgb(184, 49, 47)]dutasteride inhibits both Type 1 and Type 2 5AR.[/COLOR] [/B]General conclusions regarding the differences and similarities of these 2 agents, in terms of pharmacologic effect, safety, and efficacy, can be drawn from the evaluation of short-term comparative trials and similar but non-comparative long-term trials. [B][COLOR=rgb(184, 49, 47)]Dutasteride therapy [/COLOR]reduces [COLOR=rgb(184, 49, 47)]serum DHT significantly [/COLOR]more than finasteride.[/B] In men with benign prostatic hyperplasia (BPH), treatment with either agent results in similar prostate gland volume reduction, flow rate, and symptom improvement, and similar reductions in long-term risk of BPH development in terms of symptom progression and acute urinary retention (AUR) and BPH-related surgery. There does not appear to be any clinically significant difference between the adverse event profiles of dutasteride and finasteride. Although weak evidence suggests a difference in the onset of clinical benefit, the available non-comparative trial data do not confirm this finding. Patients with symptomatic BPH who receive dutasteride or finasteride, either as monotherapy or combination therapy with α-blockers, can expect to experience significant prostate gland size reduction, improved symptoms, and reduced risk of progression in terms of long-term adverse outcomes.[/I] [B]Figure 1 The 2 5α-reductase inhibitors (5ARIs), dutasteride and finasteride, suppress dihydrotestosterone (DHT) by inhibiting the conversion of testosterone to DHT. Finasteride inhibits only the Type 2 5AR isoenzyme, whereas [COLOR=rgb(184, 49, 47)]dutasteride, the only dual 5ARI, selectively inhibits both Type 1 and Type 2 5AR isoenzymes.[/COLOR] Data from Bartsch G et al.[/B][URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/#B1'][B]1[/B][/URL] [ATTACH type="full" alt="Screenshot (120).png"]7271[/ATTACH] [B]Figure 2 A comparative phase II evaluation of dutasteride and finasteride in a double-blind placebo-controlled trial [COLOR=rgb(184, 49, 47)]clearly demonstrates[/COLOR] that [COLOR=rgb(184, 49, 47)]serum dihydrotestosterone (DHT) suppression is significantly greater with dutasteride (0.5 mg daily) [/COLOR]than with finasteride (5 mg daily). Data from Clark RV et al.[/B][URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/#B3'][B]3[/B][/URL] [ATTACH type="full" alt="1555166095037.png"]7272[/ATTACH] [B]Conclusion [I]Without evidence from [COLOR=rgb(184, 49, 47)]long-term clinical trials comparing the safety and efficacy of dutasteride and finasteride[/COLOR], firm conclusions regarding the relative [COLOR=rgb(184, 49, 47)]efficacy and safety [/COLOR]of one agent over the other cannot be made. [/I][/B][I][B][COLOR=rgb(184, 49, 47)]However, indirect comparisons of long-term changes in prostate volume and symptoms ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/figure/F5/']Figures 5A and B[/URL]) and general conclusions drawn from the evaluation of short-term comparative trials and similar but non-comparative long-term trials can be made ([URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472914/table/T4/']Table 4[/URL]). [/COLOR]One such conclusion is that [COLOR=rgb(184, 49, 47)]dutasteride therapy reduces serum DHT significantly more[/COLOR] than finasteride. In addition, treatment with either agent results in [COLOR=rgb(184, 49, 47)]similar prostate gland volume reduction, flow rate, and symptom improvement, [/COLOR][COLOR=rgb(0, 0, 0)]and[/COLOR][COLOR=rgb(184, 49, 47)] similar reductions in long-term risk of BPH development [/COLOR][COLOR=rgb(0, 0, 0)]i[/COLOR]n terms of symptom progression and AUR and BPH-related surgery. There does not appear to be any clinically significant difference between the adverse event profile of dutasteride and finasteride. Although weak evidence suggests a difference in the onset of clinical benefit, the available non-comparative trial data do not confirm this finding. Patients with symptomatic BPH who receive dutasteride or finasteride, either as monotherapy or combination therapy with α-blockers, can expect to experience significant prostate gland size reduction, improved symptoms, and reduced risk of progression in terms of long-term adverse outcomes.[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
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Dutasteride vs Finasteride
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