The following article will review TRT and erythrocytosis and treatment options. Hypogonadism (also known as low testosterone, testosterone deficiency or androgen deficiency) is defined as biochemically having a low testosterone level in combination with specific signs and symptoms. Rarely, some people feel a little faint or lightheaded after a blood draw. There’s a small risk of infection at the site of the blood draw, especially if you have a weakened immune system. These might be shown as an absolute number of cells (written as "abs") or a percentage (%) of all of your white blood cells. Your provider can order a CBC with just total white blood cell counts or with a differential. If your provider orders a CBC with differential, it also counts the different types of white blood cells and immature cells in your sample.
A differential counts each different type of white blood cell and immature red blood cells. A complete understanding of the molecular mechanisms of testosterone-induced erythrocytosis is essential to prevention and treatment of this common and significant adverse effect of TTh. Additional factors for selecting testosterone formulations in consideration of hematologic effects include age, which is an independent risk factor for erythrocytosis in the setting of TTh . Several randomized control trials have attempted to further elucidate a relationship between DHT and testosterone-induced erythrocytosis by examining whether patients on 5α-reductase inhibitors and TTh were less likely to develop erythrocytosis .
If hematocrit is 54% or higher, stopping TRT temporarily allows levels to return to a safe range. Some people feel normal even with elevated levels, while others develop headaches, dizziness, flushing, or vision changes. Intervention usually depends on how high the levels are and whether symptoms are present. Not everyone with high hematocrit will develop complications, but the risk becomes higher as the level rises, especially above the 54% threshold.
EPO levels increased significantly during treatment with testosterone compared with placebo. Three months after discontinuation of testosterone administration, hemoglobin and hematocrit had returned to normal. This observation raises the possibility that unchanged EPO levels reflect a higher biological activity of EPO, via increased iron bioavailability, which drives erythrocytosis. Thus, understanding the mechanism of testosterone-induced erythrocytosis is important within the context of its safety, especially in older men, who experience greater increments in hemoglobin and hematocrit in response to testosterone administration than young men (4). Consistent with increased iron utilization, soluble transferrin receptor (sTR) levels and ratio of sTR/log ferritin increased significantly in testosterone-treated men. Excessively high hemoglobin/hematocrit can thicken the blood and increase the risk of clotting events. But TRT also affects your blood system, especially your hemoglobin and hematocrit levels.
Large multicenter randomized controlled trials are required to study TTh, its effects on Hb and Hct, and the clinical significance of treatment induced elevations in red blood cell mass. Wang et al. found a direct relationship between testosterone dose and the rate of erythrocytosis, which increased from 11.3% to 17.9% when increasing testosterone gel dose from 50 to 100 mg/day . Recent studies support a unified hypothesis in which testosterone formulation, dose, and pharmacokinetics collectively determine the risk of erythrocytosis by establishing the duration of supraphysiological testosterone levels . Calado et al. observed that in vitro exposure of peripheral blood lymphocytes and bone marrow to androgens increased the activity of telomerase, an enzyme involved in cell replication. Graded doses of testosterone were used to assess dose-dependent changes in hepcidin levels during 20 weeks of treatment, with findings that testosterone potently suppressed hepcidin in a dose-dependent manner. Widely debated studies by Basaria et al., Vigen et al., and Finkle et al. have observed an increased cardiovascular risk related to TTh, but these studies do not specifically correlate cardiovascular events to T-induced erythrocytosis, irrespective of their methodological flaws 16, 17, 19. It is unclear whether an increased risk would have been observed in subjects with hematocrits above a higher threshold value.
The increase in RBC’s is measured by a laboratory measurement of hemoglobin (Hgb) and hematocrit (Hct) levels. Risks of TRT include increases in estradiol levels, gynecomastia, and erythrocytosis. You might also see indices, which describe the size of your red blood cells and hemoglobin concentrations. The lab measures the amount of red blood cells, hemoglobin (the protein that carries oxygen in your red blood cells), white blood cells and platelets. A complete blood count (CBC) is a blood test that measures amounts and sizes of your red blood cells, hemoglobin, white blood cells and platelets.
In contrast to the state prior to initiating TTh, iron depletion might further compound the effect on HIFs since the PHDs require iron to catalyze prolyl hydroxylation (58). This further highlights the need for research in delineating the mechanism of action of TTh-induced erythrocytosis. The answer to this question hinges on the mechanism through which TTh induces erythrocytosis.

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