I’ve been reading. I understand that Hydroxycarbamide is used to treat both ET and PV.
If it successfully lowers red blood cells (as well as platelets) for PV patients, why is it used to treat ET where red blood cells are not excessive?
Would it cause more problems concerning red blood cells for the ET patient?
Thank you.
Hydroxycarbamide (HU) is an anti-metabolite that works by interfering with DNA activity in cells that are DNA-active. This includes hemopoietic stem cells (HSCs), endothelial and other cells. HU does not differentiate between mutated and normal HSCs. It reduces the activity of all HSCs. It thus reduces all hematopoiesis, RBCs, WBCs, and platelets. This is why anemia and immune compromise can happen with HU. It also very commonly induces macrocytosis (which is actually a benefit for people with sickle cell disease).
Here are a couple of references.
drugs.com/monograph/hydroxy...
chemocare.com/chemotherapy/....
online.epocrates.com/drugs/...
Hope that answers your question.
Thank you Hunter5582,
Having read what you sent me, I now have even more questions, and big worries.
Some things specifically listed with long term use, which, of course, applies to us.
All very difficult to accept when I only have occasional night sweat and some ringing in my ears…
I’m in utter turmoil
We all face the same kind of concerns in deciding how to treat a MPN. When do the benefits of treatment outweigh the risks inherent in the treatment. On the other hand, when does the risk of not adequately treating the MPN become the greater concern. The answer is not black and white. It is a highly individual choice. There is no one-size-fits all treatment approach. This decision needs to be based on your treatment goals, risk tolerance and preferences.
The good news is that there is more than one choice if you decide that cytoreduction is the best approach to managing ET in your case. The PEGylated interferons (e.g. Pegasys) are the other first-line treatment option. Second line treatment options include anagrelide and ruxolitinib (Jakavi).
For people who are largely asymptomatic, there is no rush to make a decision. Unless you have had a thrombotic/hemorrhagic incident or are in a high-risk group, then you can take your time to make up your mind. Note that while most hematologists follow the age-based risk protocol of high-risk=age > 60/65, not all do. Some no longer use a strictly age-based definition of risk.
Here are a few more resources you may find helpful.
mpnjournal.org/how-i-treat-...
legeforeningen.no/contentas...
mpninfo.org/conferences/202...
Please take the time to work your way through developing a knowledge base upon which to make a good decision for yourself. Knowledge is power. Know that ET can be successfully managed for a very long time. I have managed a MPN (ET that progressed to PV) for 30 years. It most certainly can be done. Know that you have this and will find an effective way to manage the ET and continue to have a good life.
I've been on HU for just over a year. I mostly had excess PLT (1000+) and it fixed that.
My red bloods were a bit high (HCT ~50) On HU my HCT stays around 43 and WBC is ok. So it is possible to get all just right with ET type blood numbers. But as Hunter says, not all get this response. And I plan to switch to Besremi for its allele fix.
I agree with everything Hunter and ETGuy have said.
I have PV and have been taking HU for two years. I tolerate it well, and it has been excellent at controlling my RBC and HCT (HCT used to be around 48>, it's now <40) WBC and Platelets are OK. Before taking HU my platelets were always normal, so I was worried about them dropping too low - close and regular monitoring by my Haem reassured me that all was well.
I had a stroke in 2012, so I knew that I needed something other than venesection and aspirin. I was always anaemic before HU (I required venesection every 6 weeks) and a normal daily life was a struggle.
My Haem wouldn't consider Interferon, as I had previously suffered a few times with depression - both periods of depression were caused by hormone imbalance. HU for me at that time was the only option.
I think hydroxy is what you might call a blunt instrument. I don't think there is something which specifically targets platelets. I have PV but my red cells were only barely raised on diagnosis. It has been possible to balance the dose to keep my platelets down without compromising my haemoglobin too much. I have done well on hydroxy over 6 years (now aged 71)
Hi, I have Et, Hydroxicarbomide lowers all blood cells. If you look at your blood test results it shows the range for each component. The aim is to lower your platelets but to keep each component in the normal range. This is why we all are so different. I’m now always anaemic and many of the components are lower or higher than they were before medication. They differ in very person but ultimately my platelets are controlled.
I am post Et Mf, and at the moment, I’m only on hydroxyurea and baby aspirin. Before this, I also took Fedratinib, and prior to that, I was taking anagrelide and Ruxo. All of these drugs, except for hydroxyurea, caused me to become anemic with constant fatigue, but did not lower my platelets, which hover between the 700’s and 800’s. With only the hu and aspirin, my hemoglobin at my last visit was 12.5, and my fatigue has greatly improved. So, in conclusion, hu has been good for me.
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