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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Erythrocytosis Following Testosterone Therapy.
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<blockquote data-quote="Nelson Vergel" data-source="post: 72568" data-attributes="member: 3"><p><strong>Erythrocytosis Following Testosterone Therapy.</strong></p><p></p><p>Review article</p><p>Ohlander SJ, et al. Sex Med Rev. 2017.</p><p></p><p>Authors</p><p>Ohlander SJ1, Varghese B2, Pastuszak AW3.</p><p>Author information</p><p>1University of Illinois at Chicago College of Medicine, Chicago, IL, USA.</p><p>2Baylor College of Medicine, Houston, TX, USA.</p><p>3Center for Reproductive Medicine, Baylor College of Medicine, Houston, TX, USA; Scott Department of Urology, Baylor College of Medicine, Houston, TX, USA. </p><p>Sex Med Rev. 2017 May 16. pii: S2050-0521(17)30041-0. doi: 10.1016/j.sxmr.2017.04.001. [Epub ahead of print]</p><p></p><p></p><p>Abstract</p><p>INTRODUCTION: A rapid increase in awareness of androgen deficiency has led to substantial increases in prescribing of testosterone therapy (TTh), with benefits of improvements in mood, libido, bone density, muscle mass, body composition, energy, and cognition. However, TTh can be limited by its side effects, particularly erythrocytosis. This review examines the literature on testosterone-induced erythrocytosis and polycythemia.</p><p></p><p>AIM: To review the available literature on testosterone-induced erythrocytosis, discuss possible mechanisms for pathophysiology, determine the significance of formulation, and elucidate potential thromboembolic risk.</p><p></p><p>METHODS: A literature review was performed using PubMed for articles addressing TTh, erythrocytosis, and polycythemia.</p><p></p><p>MAIN OUTCOME MEASURES: Mechanism, pharmacologic contribution, and risk of testosterone-induced erythrocytosis.</p><p></p><p>RESULTS: For men undergoing TTh, the risk of developing erythrocytosis compared with controls is well established, with short-acting injectable formulations having the highest associated incidence. Potential mechanisms explaining the relation between TTh and erythrocytosis include the role of hepcidin, iron sequestration and turnover, erythropoietin production, bone marrow stimulation, and genetic factors. High blood viscosity increases the risk for potential vascular complications involving the coronary, cerebrovascular, and peripheral vascular circulations, although there is limited evidence supporting a relation between TTh and vascular complications.</p><p></p><p>CONCLUSION: Short-acting injectable testosterone is associated with greater risk of erythrocytosis compared with other formulations. The mechanism of the pathophysiology and its role on thromboembolic events remain unclear, although some data support an increased risk of cardiovascular events resulting from testosterone-induced erythrocytosis. Ohlander SJ, Varghese B, Pastuszak AW. Erythrocytosis Following Testosterone Therapy. Sex Med Rev 2017</p></blockquote><p></p>
[QUOTE="Nelson Vergel, post: 72568, member: 3"] [B]Erythrocytosis Following Testosterone Therapy.[/B] Review article Ohlander SJ, et al. Sex Med Rev. 2017. Authors Ohlander SJ1, Varghese B2, Pastuszak AW3. Author information 1University of Illinois at Chicago College of Medicine, Chicago, IL, USA. 2Baylor College of Medicine, Houston, TX, USA. 3Center for Reproductive Medicine, Baylor College of Medicine, Houston, TX, USA; Scott Department of Urology, Baylor College of Medicine, Houston, TX, USA. Sex Med Rev. 2017 May 16. pii: S2050-0521(17)30041-0. doi: 10.1016/j.sxmr.2017.04.001. [Epub ahead of print] Abstract INTRODUCTION: A rapid increase in awareness of androgen deficiency has led to substantial increases in prescribing of testosterone therapy (TTh), with benefits of improvements in mood, libido, bone density, muscle mass, body composition, energy, and cognition. However, TTh can be limited by its side effects, particularly erythrocytosis. This review examines the literature on testosterone-induced erythrocytosis and polycythemia. AIM: To review the available literature on testosterone-induced erythrocytosis, discuss possible mechanisms for pathophysiology, determine the significance of formulation, and elucidate potential thromboembolic risk. METHODS: A literature review was performed using PubMed for articles addressing TTh, erythrocytosis, and polycythemia. MAIN OUTCOME MEASURES: Mechanism, pharmacologic contribution, and risk of testosterone-induced erythrocytosis. RESULTS: For men undergoing TTh, the risk of developing erythrocytosis compared with controls is well established, with short-acting injectable formulations having the highest associated incidence. Potential mechanisms explaining the relation between TTh and erythrocytosis include the role of hepcidin, iron sequestration and turnover, erythropoietin production, bone marrow stimulation, and genetic factors. High blood viscosity increases the risk for potential vascular complications involving the coronary, cerebrovascular, and peripheral vascular circulations, although there is limited evidence supporting a relation between TTh and vascular complications. CONCLUSION: Short-acting injectable testosterone is associated with greater risk of erythrocytosis compared with other formulations. The mechanism of the pathophysiology and its role on thromboembolic events remain unclear, although some data support an increased risk of cardiovascular events resulting from testosterone-induced erythrocytosis. Ohlander SJ, Varghese B, Pastuszak AW. Erythrocytosis Following Testosterone Therapy. Sex Med Rev 2017 [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Erythrocytosis Following Testosterone Therapy.
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