I’ve been on TRT for a little over 1.5yrs; take 125mg/wk on a M,W,F injection (test cyp). Had my bloods done a few weeks ago and everything good with all markers other than test was just over lab range (to be expected when taking exogenous).
However, I just spent the last 24hrs in the hospital with bilateral pulmonary embolism that is being attributed to increased red blood cell and hematocrit from TRT. Dr wants me to stop all together, hematologist, not as adamant; following up with him in the next couple weeks. For now, I’m on double dose of blood thinners.
Anybody experience this?
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I had a bilateral PE before I started TRT. Stay on the blood thinners and you’ll be good. You must have a genetic predisposition like factor5 leiden. You MUST have your Dr test for genetic mutations. PE has a very high deathrate. Somewhere around coin flip. You are blessed to still be here.
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This^
Now that I’ve been released from the hospital, and have access to my computer, i can share my labs for reference.
As mentioned the GP at the hospital was adamant that testosterone was the cause and i should cease all treatment immediately, but when she talked to the hematologist, he was less adamant and i have a follow up with him in a week or two. So hopefully i can stay on TRT and add a thinner to my regime, but we will see.
Did they check INR blood test?
Did you have covid or take the vaccine? That could have caused the clot.
Your GP full of crap. Your blood isn’t thick. Hematocrit is perfectly fine. Are you on Anastrozole? That medication has been linked to clotting. You need the genetic testing. The hematologist should be digging deeper. As long as you are on the blood thinners you are good.
INR was not tested; not something my nurse practitioner typically checks for. But i am sure the hematologist will.
I am prescribed arimidex, but don’t generally take it. I have taken 1/4mg a week in the past briefly, any more than that and i get pimples and ED issued that don’t resolve with cialis
Get lab results from hospital. They must have checked that and more
Shortly after taking TRT, My blood got thicker as result I take Xarelto 20mg. every day at 10am, per my Cardiologist. My Brother takes Warfarin 4mg every day per his Hematologist. Our Dr.'s told us the potential clots will cause us a stroke or heart attack. I cannot stop the TRT due to other health issues with my Pituitary. My Brother started clotting soon after beginning TRT too. We believe its in our DNA on my Mothers side. One must get labs done regularly. Don’t cheat yourself. Both of my legs filled with clots. They are gone now since taking Xarelto…
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What lab determines clotting?
The d-dimer blood test will test how long it takes for blood to clot. If your blood is extra thick it will clot too quick. If you are on too high a dose of blood thinners it will take too long to clot. It’s not a test for genetic mutations.
Factor V lieden is a common one but there are other genetic mutations to test for. If you are heterozygous you have an elevated chance (5-6x) of developing DVT. If you are homozygous you have a much greater chance, I think about 100X. This is actually tested in 23andme. I was diagnosed with the heterozygous mutation of Factor V Lieden by the hematologist along with another mutation and then years later I did 23andme and it caught both of them.
This topic is close to my heart since I almost died from a PE about 5 years ago. Shit was crazy. I was a totally healthy male and then the next day I was laid out in the ICU for a week fighting for my life. I’m a veteran, been in warzones for several years and I never felt so mortal and out of control in my life as I did that week in the hospital.
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Factor V lieden is rough. My Mother and one of my brothers have Factor 5, its a lifetime of Warfarin with monthly PT-Inr tests. Forget the daily dose and it could be real trouble. You also have to watch what foods you eat. Some will cause you to hemorrhage. I’ve seen this happen with my Mother. I was tested 2X for Factor 5 , both came back Neg. My Mother is 94 and I take her to Quest Labs every month.
to be honest, if we didn’t have to do covid screening before going to work, which i failed due to a shortness of breath symptom. Subsequently, i had to go for covid testing. The doctor at the clinic told me i should go to the hospital to get checked out and he would call ahead to let them know i was coming.
Had it not been for those two events, i would’ve just tried to suck it up and push through it and likely would’ve been found a week later in my basement gym.
There is a lot of “don’t worry about RBC or hematocrit” talk on here, but I have not read much about the clotting risks; i consider myself very lucky
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Good advice. Your post made me book an appointment with a hematologist. Just to cover my bases. Proactive.
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Wow. That’s serendipity. Life is so crazy.
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Thank you for the warning. You are absolutely correct that the blanket, unqualified statement that elevated Hct is harmless is an extremely irresponsible message.
I am so glad you are doing better. Take care. And thank you for taking the time to share your experience!
Can’t use Hct as an absolute proxy for blood viscosity. It is only correlated. We’d have to understand each individual’s inflammation and plasma protein status to make a reasonable inference about whole blood viscosity from Hct alone. That’s why one guy can run an Hct of 55 and feel perfectly fine and another with Hct of 51 may feel much worse.
Exactly. That’s why his GP is wrong for blaming it on hematocrit well within normal ranges
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How is this a hematocrit issue when its clearly within range? You’re all going to ignore the data to fit a reason for someones health scare, without actual evidence for the cause? Im not convinced TRT is the cause.
I think we are all in violent agreement here actually. It’s not at all clear that TRT or Hct was the cause although previous study has shown correlation between Hct and VT (not causation between Hct and VT). See this review and paper cited therein. So I am agreeing that the Provider above may have little evidence to throw the event at TRT/Hct but worth being cautious since we don’t completely understand it.
As stated previously many many times, primary concern with elevated Hct would be potential wear and tear on the heart but clotting issues do get discussed and correlate with elevated Hct. The rub is that both clotting and elevated Hct may be correlated to another (not fully understood) cause(s).
An increased risk of venous and arterial thrombosis in relation to primary erythrocytosis has been well described. However, the mechanisms are complex and being debated14 and a direct relation between the hematocrit level and the risk of venous thrombosis is not clearly present in these conditions. An old study from 1978 found a striking correlation between hematocrit level and thrombosis in patients with polycythemia vera,15 but this correlation was not confirmed in a recent study in which no such relation could be demonstrated.16
With respect to the association of venous thrombosis with hematocrit in the general population, data are scarce and inconclusive. Vaya et al. performed a case-control study in 109 patients with a first deep vein thrombosis, without thrombophilia, and 121 healthy controls. They reported that the percentage of cases with a hematocrit above 45% was higher in cases than in controls, i.e. 43% versus 27%. The association was attenuated when several other factors were included in a multivariate model.17 In one other population-based study (the LITE study, a cohort study in subjects above 45 years of age), no relation between high hematocrit levels and risk of venous thrombosis was demonstrated, but the authors used a relatively low cut-off level for the hematocrit (43.5%).18
The strengths of the new study by Braekkan and colleagues are that it is large, prospective, and carried out in a general population with a high response rate, a long follow-up, and well-validated venous thrombotic events.2 We may, therefore, assume that the link found between high hematocrit and risk of venous thrombosis is real, but again, the important issue is to decide whether or not the relation is causal or explained by other diseases.
Hematocrit is one of the major determinants of blood viscosity,5 and increases in the hematocrit might favor clot formation by increasing the residence time of circulating platelets and coagulation factors adjacent to dysfunctional endothelium. Furthermore, elevated hematocrit has been shown to promote the transport of platelets towards the vessel wall, thereby increasing the interaction with the vasculature.23 Blood clotting is also dependent on the velocity gradient at which the clotting takes place. The influence of the hematocrit on blood viscosity increases when the shear rate decreases.5,24 Under low-flow conditions, such as in the venous system, increases in hematocrit may have a strong influence on blood flow and, thereby, clinical outcome.
RBC mass may also have a direct effect on thrombotic mechanisms. A recent experimental study investigating the effect of RBC on thrombin generation, showed that the total amount of thrombin activity generated, and the maximum concentration of thrombin achieved, was proportional to the hematocrit.25 RBC may also take part in thrombus formation by other mechanisms, such as stimulation of platelet aggregation through ADP release,26–28 or possibly through the exposure of phosphatidylserine.29
The main strengths of our study are its prospective design, the large number of participants recruited from a general population with high attendance rate, the long-term follow-up, and the validation of the venous thromboembolic events. All hospital care and radiological imaging in the region is provided exclusively by a single hospital, which enhances the possibility of a complete VTE registry. However, the study has some limitations. Modifiable risk factors, such as hematocrit and related hematologic variables, are a potential weakness of cohort studies, especially when the time between exposure and disease manifestation is long. However, this type of non-differential misclassification generally leads to underestimation of the true associations. In our study, smoking was assessed as a dichotomous variable (current smoker: yes/no). Thus, we were unable to take into consideration the potential dose-dependent effect of smoking on hematocrit, and thereby unable to remove all possible confounding by smoking. Underlying medical conditions such as lung, heart and kidney diseases can influence the level of hematocrit. In our study, information on other medical conditions was only available for those who developed VTE. In men, the presence of other medical conditions did not differ across various levels of hematocrit ( data not shown ). In women, the presence of other medical conditions was slightly higher among those whose hematocrit was in the upper 20th percentile. Since there was no available clinical information on underlying disease during follow-up in the reference group, we did not have sufficient clinical information for the total population to consider underlying disease as a possible cause of high hematocrit and risk of thrombosis in detail.
In conclusion, hematocrit and the related variables hemoglobin and RBC count were identified as risk factors for VTE in our prospective, population-based study. The size of red blood cells, expressed as MCV, was not associated with VTE. Our findings may suggest that hematocrit should be taken into consideration for risk assessment in VTE.
just to clarify, as readalot puts far more eloquently and intelligently than I could ever articulate. I don’t believe that Hct is to blame here (especially since the bloodwork was taken at 3pm after having absolutely nothing to drink all day, i’m not surprised that Hct would be artificially elevated), but I mentioned it to bring awareness, not to ignore all measurables.
To be honest, I stopped visiting this forums several months ago due to the “you’re not doing the same as me, therefore you are stupid and wrong” mentality that seems to be prevalent in the vocal minority
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