Marco,
Hopefully your physician did a coagulopathy work-up on you (or referred you to a hematologist that did) following your blood clot episodes BEFORE giving you that script for testosterone.
Testosterone replacement, in some unfortunate men, can lead to the discovery of an underlying coagulopathy (like Factor V Leiden) after the fact...ie: after they develop a blood clot. This is not very common, but common enough to be worrisome especially with your history of clotting.
Dr Saya
Thanks for chiming in, Dr. Saya.
We have run every coagulation test known and even some esoteric thrombosis panels (Labcorp and Esoterix). Am +/+ (homozygous carrier) for MTHFR C677T which can cause clots if homocysteine is elevated, but my HCY is consistently normal (average: 7.5) as I've addressed it with methylfolate, methylB12, etc.
I am also +/- (heterozygous carrier)for the PAI-1 gene which puts me at intermediate risk for thrombosis, but the hemo does not think this is clinically significant. We also ruled out all other genetic causes (am negative for FVL, protein C, S, APS, etc.) however, my FVIII, d-dimer and other acute phase reactors have remained elevated. Again, the hemo did not think these were clinically significant (which means to me, he doesn't know). I am now thinking there is an immune component (e.g. chronic infection) that is causing the hypercoagulable state. as I have some past exposure to pathogens that my immune system may not have resolved (low normal WBC/NK cells). My Lp(a) and CRP are also elevated. I have read that elevated Lp(a) can put one at risk for clotting s well. TRT helps bring Lp(a) and inflammation down.
So, at this point, we don't know have a cause.
In my research, the only documented risk factors with respect to clots lie in the management (or mismanagement) of E2 and prevention of polycythemia.
Some recent studies:
http://www.ncbi.nlm.nih.gov/pubmed/23925401
http://cat.sagepub.com/content/early...85154.abstract
"In 60 men on testosterone, 20 (33%) had high estradiol (E2 >42.6 pg/mL). When exogenous testosterone is aromatized to E2, and E2-induced thrombophilia is superimposed on thrombophilia-hypofibrinolysis, thrombosis occurs."
We all know that management of E2 and polycythemia is mandatory while on TRT, but how much of other factors could play into this equation???
These studies show that androgen deficiency can be a cause of low fibrinolysis and other elevated blood factors:
http://www.ncbi.nlm.nih.gov/pubmed/8844628
http://www.ncbi.nlm.nih.gov/pubmed/18591887
I am clearly deficient in free T and E2 and need treatment. Knowing this history is one of the major reasons I've been holding off with TRT. I would hate to go back on a thinner like coumadin just so I can do TRT. At this point, I actually need T to aromatize to E2.
Bottom line: Since T has both pro- and anti-thrombotic effects, my sense is that for those of us that have hypercoagulation issues, extreme vigilance need be implemented in the monitoring of E2, CBC, and follow-up blood factors.
When it comes to HRT, I have found hemos to be a waste of time. They automatically relegate it as a contraindication and know zip about it.
By the way, do you/
Defy have access to injectable methylfolate (L-5-MTHF)?