Platelets contain the androgen receptor. If they make T when there is none in circulation, I imagine that it is for their own needs. It would be odd if PCa tumors could enlist the help of platelets, but who knows?
"Platelets have been postulated to perform a critical function in the pathogenesis of prostate cancer for decades ..."
This is misleading, I feel. Platelets have a role in the abnormal coagulation that seems to be necessary for metastasis. No other role has been suggested.
If PCa is able to steal platelet T, what can we do?
The trend in drug research is to silence alternative sources of T. I don't know why doctors ignore statins, in this regard. When T is scarce, cells may make their own from cholesterol - & might even synthesize their own cholesterol. It seems prudent to be on a statin when starting ADT.
I'm not a chemist and may have misunderstood what I've read, but I read that all tissues in the human body that produce testosterone do it using the same or similar biochemical "pathway", i.e., they convert compound A into B in one chemical reaction, B into C via another reaction, and so on with a stage somewhere down the line where the product of the reaction is testosterone. Zytiga (abiraterone) supposedly interferes with one of the reactions found in every cell that produces testosterone, no matter whether it's in the testes, the adrenal gland, the blood platelets, or wherever. So in theory, taking Zytiga should solve the blood platelet problem, if it is a problem.
I've wondered of late whether patients would do better if started on Zytiga or Xtandi, or at least Firmagon (degralix), rather than the traditional LHRH agonists - Lupron, Zoladex, and Eligard.
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.