High haematocrit on testosterone: what level is a concern and how it is monitored

On testosterone treatment, haematocrit becomes a concern once it goes above 52% (or haemoglobin above 18.5 g/dL), which is how erythrocytosis is defined in men. The Endocrine Society's 2018 guideline sets the threshold for action at 54%: above that, treatment is stopped until the level comes down. To catch it early, haematocrit is measured before starting, at 3-6 months and then once a year.

Behind those figures there is a well-understood mechanism, some risk data that need to be read with care, and a monitoring schedule that in Spain is set out both in the summary of product characteristics and in the pharmacovigilance information. Let's take it step by step.

What haematocrit is and why testosterone raises it

Haematocrit is the percentage of your blood volume taken up by red blood cells. If it rises too much, the blood becomes thicker, which is why it is monitored with any treatment that stimulates red cell production. Testosterone is one of those treatments, and it works through two complementary routes.

• Erythropoietin (EPO): testosterone increases this kidney hormone, which signals the body to make red blood cells, and it also changes its set point. In other words, the body keeps EPO higher than normal for the same level of haemoglobin, as if the thermostat had been turned up a few degrees.
• Available iron: with testosterone doses above replacement level, hepcidin, the protein that limits the release of iron into the blood, falls by more than 50% within 7 days, according to the work of Bachman and colleagues. As hepcidin falls, ferroportin, the channel that releases iron, increases, and the bone marrow has more raw material to make red blood cells.

That is why some rise in haematocrit is an expected effect of treatment and does not, on its own, mean there is a problem. What matters is how much it rises and in what context.

Secondary erythrocytosis, not polycythaemia vera

The terminology is easy to mix up. High haematocrit caused by testosterone is a secondary erythrocytosis: red blood cells increase in response to an external stimulus, in this case the hormone. Polycythaemia vera is something else entirely, a bone marrow disease that produces red blood cells autonomously and is investigated and treated differently. The fact that some texts call it secondary polycythaemia does not turn one into the other.

When it becomes a concern: the 52% and 54% thresholds

In practice, two figures are used. The review by Ohlander and colleagues defines testosterone-induced erythrocytosis as a haematocrit above 52% or a haemoglobin above 18.5 g/dL. The Endocrine Society, in its 2018 guideline, places the action point at 54%: if it is exceeded, it recommends stopping treatment until the level comes down, ruling out other causes that also raise haematocrit, such as hypoxia or sleep apnoea, and restarting at a lower dose.

It is worth knowing that these thresholds do not come from an exact biological cut-off. The editorial accompanying the study by Ory and colleagues notes that the haematocrit values used in guidelines appear to have been chosen arbitrarily. There is no figure above which thrombosis is certain, nor one below which the risk is zero: they are practical limits for deciding when to act.

What risk has actually been measured

The most widely cited data come from the retrospective study by Ory and colleagues, published in The Journal of Urology in 2022. They compared two groups of 5,842 men on testosterone treatment: one group developed polycythaemia (haematocrit above 52%) and the other did not. In the first year, the rate of major adverse cardiovascular events or venous thrombosis was 5.15% in the polycythaemia group versus 3.87% in the group without it, an odds ratio of 1.35 (95% CI 1.13-1.61).

There are two important caveats. It is an observational study, so it shows an association and does not by itself prove that haematocrit is the cause. And in the same study, men who did not develop polycythaemia had no greater cardiovascular or thrombotic risk than untreated men with hypogonadism. Read this way, the message is not that testosterone is dangerous in itself, but that a high haematocrit is a signal that deserves monitoring.

The TRAVERSE trial (NEJM, 2023) provides the other half of the picture. In 5,246 men aged 45 to 80 with hypogonadism and cardiovascular risk or a history of cardiovascular disease, testosterone was no worse than placebo for major adverse cardiovascular events (7.0% versus 7.3%). However, the treated group had more atrial fibrillation, acute kidney injury and pulmonary embolism. It is reassuring as far as heart attack and stroke are concerned, but it does not allow us to say the treatment is harmless, and the sources consulted do not report haematocrit data from that trial.

Not all forms of testosterone raise it equally

The route of administration matters. According to the Ohlander review, short-acting testosterone injections cause more erythrocytosis than gels and other forms, probably because they produce sharper hormone peaks after each injection. That does not mean gel cannot raise haematocrit: it can, and it is monitored too. If you want to see what else differs between one format and another, we explain it in testosterone gel versus injections.

In CIMA, the medicines database of the Spanish Agency of Medicines and Medical Devices (AEMPS), there are summaries of product characteristics for injectable testosterone undecanoate (Reandron) and for testosterone gel (Testogel). Testosterone cipionate (Testex Prolongatum) had a supply problem that the AEMPS reported in 2017, and its current availability in Spain needs to be checked in CIMA. For undecanoate, the Spanish safety information warns of two specific risks: polycythaemia and pulmonary oil microembolism, the latter related to the oily solution of the injection.

How haematocrit is monitored during treatment

The check itself is simple: a full blood count in a routine blood test. What gets agreed is the schedule, and the sources are fairly consistent.

• Endocrine Society (2018): haematocrit before starting treatment, at 3-6 months and then once a year.
• Spanish safety information on undecanoate: blood tests before starting, at 3-4 months and at 12 months during the first year, and then once a year.
• Summary of product characteristics in CIMA: periodic monitoring of haemoglobin and haematocrit, liver function and lipids during long-term androgen treatment, with possible dose adjustment if levels rise.

The baseline test is the starting point: without a baseline value, there is no way to know how much it has risen afterwards. It is part of the initial work-up we describe in which blood tests you need before testosterone is prescribed, alongside other tests such as PSA.

If haematocrit comes back high at a check-up, the Endocrine Society guideline sets out what the doctor considers: pausing treatment until it comes down, looking for other causes such as sleep apnoea and, where appropriate, restarting at a lower dose. It is a clinical decision that takes into account the rest of the blood results, the form of administration and each person's history. This is also the main problem with using testosterone on your own: without monitoring, nobody is watching the haematocrit, and we discuss that risk in testosterone without a prescription and online sellers.

Key takeaways and next steps

Testosterone raising haematocrit is a known effect that is easy to monitor: it becomes a concern above 52%, action is taken from 54%, and it is checked with blood tests at agreed points, especially during the first year. The risk is real, but it is managed through follow-up, not left to chance. If you suspect your testosterone is low, what is available in Spain is medical treatment with a prior assessment, prescription by a registered doctor where appropriate, and ongoing monitoring; that is what AiON offers through its men's hormonal health treatment. You can check in a few minutes whether you are eligible.