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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Should We Be Managing Estradiol and Hematocrit in Men on Testosterone Replacement?
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<blockquote data-quote="Dr Justin Saya MD" data-source="post: 71285" data-attributes="member: 12687"><p>Off the current topic, but since you mentioned it I'll address. I actually treat females as well and have been since day 1. Unfortunately there is indeed data on increased coagulability with oral estradiol (and yes of course we know the story with Premarin/Prempro, etc...preaching to the choir there). </p><p></p><p><a href="https://www.ncbi.nlm.nih.gov/m/pubmed/11341495/#fft" target="_blank">https://www.ncbi.nlm.nih.gov/m/pubmed/11341495/#fft</a></p><p></p><p>"oral estradiol (2mg) changed markers of coagulation towards hypercoagulability, and increased serum CRP concentrations."</p><p></p><p>This from ACOG (American College of Obstetricians and Gynecologists):</p><p></p><p>"In most investigations of the relationship of venous thromboembolism and menopausal HT, the route of hormone administration has been primarily oral. It has been proposed that orally administered estrogen may exert a prothrombotic effect through the hepatic induction of some of these substances (18–23). The prothrombotic effect is possibly related to high concentrations of estrogen in the liver due to the “first-pass” effect. Studies that compared oral and transdermal ET have demonstrated that transdermally administered estrogen has little or no effect in elevating prothrombotic substances and may have beneficial effects on proinflammatory markers, including C-reactive protein, prothrombin activation peptide, and antithrombin activity. Also, in contrast to oral ET, transdermal ET also may have a suppressive effect on tissue plasminogen activator antigen and plasminogen activator inhibitor activity (23–29).</p><p></p><p>The Estrogen and Thromboembolism Risk study, a multicenter case–control study of thromboembolism among postmenopausal women aged 45–70 years, demonstrated an odds ratio for venous thromboembolism in users of oral and transdermal estrogen to be 4.2 (95% CI, 1.5–11.6) and 0.9 (95% CI,0.4–2.1), respectively, when compared with nonusers (10). Transdermal estrogen had no increased risk compared with nonusers. Similar results were reported elsewhere (30–35) and of particular importance, in women who were stratified for weight (36) and the presence of prothrombotic mutations (37).</p><p></p><p>Several nonoral delivery systems presently are available for the administration of estradiol. These include transdermal estradiol patches, ethanolic estradiol-containing gels and sprays, and the vaginal (ring) delivery system. Topical vaginal creams and tablets prescribed for treatment of local urogenital atrophic changes have low levels of systemic absorption but have no detectable effect on coagulation proteins or incidence of venous thromboembolism. Both transdermal (patches or gels) and vaginal (ring) delivery bypass the gastrointestinal conversion of estradiol to estrone with less increase of triglyceride levels, clotting factors, and globulins (38). The vaginal ring containing estradiol acetate for systemic treatment, shown to be effective in the management of vasomotor symptoms, is not associated with an increased risk of venous thromboembolism (38–40). The practicing gynecologist should be aware that other less mainstream estrogen delivery methods, including transbuccal lozenges and troches, are widely used throughout the United States. These alternatives, which are meant to dissolve in the mouth and bypass the enterohepatic circulation, are available as single agents or in combination with other hormones and are fashioned by compounding pharmacies. Data on the safety and efficacy of compounded troches and lozenges are limited. Although widely prescribed, these less mainstream estrogen delivery methods have not been subjected to significant scientific scrutiny."</p><p></p><p>Since this relates to females only (as no males will be taking any estradiol, let alone oral vs transdermal), we'll not sidetrack the thread any further on that topic.</p></blockquote><p></p>
[QUOTE="Dr Justin Saya MD, post: 71285, member: 12687"] Off the current topic, but since you mentioned it I'll address. I actually treat females as well and have been since day 1. Unfortunately there is indeed data on increased coagulability with oral estradiol (and yes of course we know the story with Premarin/Prempro, etc...preaching to the choir there). [url]https://www.ncbi.nlm.nih.gov/m/pubmed/11341495/#fft[/url] "oral estradiol (2mg) changed markers of coagulation towards hypercoagulability, and increased serum CRP concentrations." This from ACOG (American College of Obstetricians and Gynecologists): "In most investigations of the relationship of venous thromboembolism and menopausal HT, the route of hormone administration has been primarily oral. It has been proposed that orally administered estrogen may exert a prothrombotic effect through the hepatic induction of some of these substances (18–23). The prothrombotic effect is possibly related to high concentrations of estrogen in the liver due to the “first-pass” effect. Studies that compared oral and transdermal ET have demonstrated that transdermally administered estrogen has little or no effect in elevating prothrombotic substances and may have beneficial effects on proinflammatory markers, including C-reactive protein, prothrombin activation peptide, and antithrombin activity. Also, in contrast to oral ET, transdermal ET also may have a suppressive effect on tissue plasminogen activator antigen and plasminogen activator inhibitor activity (23–29). The Estrogen and Thromboembolism Risk study, a multicenter case–control study of thromboembolism among postmenopausal women aged 45–70 years, demonstrated an odds ratio for venous thromboembolism in users of oral and transdermal estrogen to be 4.2 (95% CI, 1.5–11.6) and 0.9 (95% CI,0.4–2.1), respectively, when compared with nonusers (10). Transdermal estrogen had no increased risk compared with nonusers. Similar results were reported elsewhere (30–35) and of particular importance, in women who were stratified for weight (36) and the presence of prothrombotic mutations (37). Several nonoral delivery systems presently are available for the administration of estradiol. These include transdermal estradiol patches, ethanolic estradiol-containing gels and sprays, and the vaginal (ring) delivery system. Topical vaginal creams and tablets prescribed for treatment of local urogenital atrophic changes have low levels of systemic absorption but have no detectable effect on coagulation proteins or incidence of venous thromboembolism. Both transdermal (patches or gels) and vaginal (ring) delivery bypass the gastrointestinal conversion of estradiol to estrone with less increase of triglyceride levels, clotting factors, and globulins (38). The vaginal ring containing estradiol acetate for systemic treatment, shown to be effective in the management of vasomotor symptoms, is not associated with an increased risk of venous thromboembolism (38–40). The practicing gynecologist should be aware that other less mainstream estrogen delivery methods, including transbuccal lozenges and troches, are widely used throughout the United States. These alternatives, which are meant to dissolve in the mouth and bypass the enterohepatic circulation, are available as single agents or in combination with other hormones and are fashioned by compounding pharmacies. Data on the safety and efficacy of compounded troches and lozenges are limited. Although widely prescribed, these less mainstream estrogen delivery methods have not been subjected to significant scientific scrutiny." Since this relates to females only (as no males will be taking any estradiol, let alone oral vs transdermal), we'll not sidetrack the thread any further on that topic. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Should We Be Managing Estradiol and Hematocrit in Men on Testosterone Replacement?
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