Erythrocytosis Following Testosterone Therapy.

[Nelson Vergel]

Erythrocytosis Following Testosterone Therapy.

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

 

[Eli1947]

Nelson Vergel , did you had a chance to read the article and find out what is the mechanism by which Testosterone cause the Erythrocytosis?
In my case I reached this stage though erythropoitien is low , JAK2 mutations none detected and T protocol T-enanthrate 0.25-0.3 ml/w eg 82-75 mg/W.

 

[Tommy Wall]

Testosterone propionate is a fast-acting ester. Testosterone enanthate and testosterone cypionate are slow-acting injectable forms.
Meaning that the latter ones are not included in the above article or?

 

[Nelson Vergel]

Testosterone propionate is a fast-acting ester. Testosterone enanthate and testosterone cypionate are slow-acting injectable forms.
Meaning that the latter ones are not included in the above article or?

all esters and testosterone creams/gels cause increased red blood cells (maybe in different degrees)

 

[Eli1947]

all esters and testosterone creams/gels cause increased red blood cells (maybe in different degrees)

I thought Testosterone induces production of red blood cells via eryhropoitine production . But low levels of it with moderate testosteroe levels near 20nmole/L at peak make me to wonder about the mechanism of vaction. Through about 6 years of treatment hematocrit went up from about 40 to 54.7%.