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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Pharmacogenetics of testosterone replacement therapy
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<blockquote data-quote="madman" data-source="post: 226739" data-attributes="member: 13851"><p><em><strong>*</strong><em><strong>Men presenting with features of hypogonadism may exhibit normal testosterone levels but CAG repeat lengths above the normal average (Europe: 21, Africa: 17, Asia: 23): <u>hence, a CAG repeat length longer than 25 is still considered to be within the normal range, but can already be associated with reduced androgen action and accompanying clinical features, suggesting classical hypogonadism in the case of still normal testosterone concentrations</u></strong></em></em></p><p><em><em><strong></strong></em></em></p><p><em><em><strong><em><strong>*A <u>strictly defined threshold to hypogonadism is likely to be replaced by a continuum spanned by genetics as well as symptom specificity</u>. In addition, the effects of externally applied testosterone can be markedly influenced by the (CAG)n and respective pharmacogenetic implications are likely to influence indications as well as modalities of testosterone treatment of hypogonadal men</strong></em></strong></em></em></p><p><em><em><strong><em><strong></strong></em></strong></em></em></p><p><em><em><strong><em><strong>*<strong><em>It should be mentioned that <u>many other factors are most likely to be influencing testosterone action</u>, be it the endogenous hormone or exogenously administered androgens</em></strong></strong></em></strong></em></em></p><p><em><em><strong><em><strong><strong><em></em></strong></strong></em></strong></em></em></p><p><em><em><strong><em><strong><strong><em>*<strong><em>The <u>CAG repeat polymorphism</u> cannot be the only determining factor in androgen sensitivity</em></strong></em></strong></strong></em></strong></em></em></p><p><em><em><strong><em><strong><strong><em><strong><em></em></strong></em></strong></strong></em></strong></em></em></p><p><em><em><strong><em><strong><strong><em><strong><em>*<em><strong>The <u>level of knowledge required to include the AR gene CAG repeat polymorphism into routine andrological assessments is not sufficient</u>, but it has become a clinically and scientifically worthy concept to determine the CAG repeat length in subjects with normal testosterone levels and unexplained features of hypoandrogenism.</strong></em></em></strong></em></strong></strong></em></strong></em></em></p><p><em></em></p><p><em><strong>*In summary, <u>a confined and universal threshold for testosterone levels to hypogonadism does not exist</u>, but, instead, individual thresholds of testosterone levels according to the length of the CAG repeat polymorphism are likely to be of clinical relevance</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 226739, member: 13851"] [I][B]*[/B][I][B]Men presenting with features of hypogonadism may exhibit normal testosterone levels but CAG repeat lengths above the normal average (Europe: 21, Africa: 17, Asia: 23): [U]hence, a CAG repeat length longer than 25 is still considered to be within the normal range, but can already be associated with reduced androgen action and accompanying clinical features, suggesting classical hypogonadism in the case of still normal testosterone concentrations[/U] [I][B]*A [U]strictly defined threshold to hypogonadism is likely to be replaced by a continuum spanned by genetics as well as symptom specificity[/U]. In addition, the effects of externally applied testosterone can be markedly influenced by the (CAG)n and respective pharmacogenetic implications are likely to influence indications as well as modalities of testosterone treatment of hypogonadal men *[B][I]It should be mentioned that [U]many other factors are most likely to be influencing testosterone action[/U], be it the endogenous hormone or exogenously administered androgens *[B][I]The [U]CAG repeat polymorphism[/U] cannot be the only determining factor in androgen sensitivity *[I][B]The [U]level of knowledge required to include the AR gene CAG repeat polymorphism into routine andrological assessments is not sufficient[/U], but it has become a clinically and scientifically worthy concept to determine the CAG repeat length in subjects with normal testosterone levels and unexplained features of hypoandrogenism.[/B][/I][/I][/B][/I][/B][/B][/I][/B][/I] [B]*In summary, [U]a confined and universal threshold for testosterone levels to hypogonadism does not exist[/U], but, instead, individual thresholds of testosterone levels according to the length of the CAG repeat polymorphism are likely to be of clinical relevance[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Pharmacogenetics of testosterone replacement therapy
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