I have been diagnosed with ET jak2+ for 5 years following a heart attack where they found my platelets were at 1 million. The hospital did not alert me but my GP did at my 1 month follow up visit. I was sent to a hematologist/oncologist. I was put on Hydrea 500mg 7 tabs a week eventually increased to 10 tabs a week until my platelets were down under 400. I am now in a new state, new Dr which happens to be an MPN specialist and my numbers have been slowly increasing and I am concerned. My platelets as of 2 months ago were over 500 and when I mentioned I was concerned she stated there is new research that states that increased platelets do not cause thrombosis. Well, this is how I found out I had ET because of a thrombotic event. Has anyone else heard this new information?
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You're right that PLT limits are all over the place. My provider uses 369, some Drs are ok to 600. Current info is confusing on this risk, so your Dr is consistent there. But this is still standard practice:
<<Antiplatelet therapy is recommended in all patients aged ⩾ 60 years and in those with a positive history of thrombosis or with cardiovascular risk factors>>
If your PLT keeps rising that seems a further reason to consider it.
Here is a page with a risk calculator using IPSET-t risk. Probably too simple but a guide.
Thank you for the articles. I did the test and I am high risk due to age and CAD with a 50% blockage in the LAD(widow maker or in my case widower maker) I found out about the blockage due to the heart attack and was just prior to my ET diagnosis.
That is actually not new information. There is no linear relationship between platelet levels and risk of thrombosis. The only linear relationship is between platelet levels and risk of hemorrhage. When platelet levels go above a certain level there is a risk of Acquired von Willebrand Disease (a bleeding disorder). There can also be issues with increased hemorrhage short of AcqvWBD. The odd thing with thrombocytosis is that we are at risk for both thrombosis and hemorrhage. We are also at risk for microvascular symptoms, which are not the same as thrombosis.
The reason for all this has to do with how the blood cells behave. This is more than simply how many of them there are. The interaction between blood cells, interaction with the vascular endothelium, and the mechanisms for coagulation are all part of the picture. It appears that the JAK2 mutation makes the blood cells "extra sticky." At the same time. alterations in von Willebrand factors and other alterations can also cause bleeding/bruising and microvascular issues like erythromelalgia. .
Note that is is normal for platelet levels to vary by as much as 100 in a single day as a reaction to what is going on in your body. It is always the trend over time that matters, never a single lab read. There is no significant difference in risk of thrombosis between 400 and 500. EPguy is correct that some MPN Specialist now use 600 as the cytoreduction target.
There is an emerging view that absolute numbers of platelets are not the appropriate target. What may matter more is the delta (degree of change). There is also an understanding that treatment goals can vary by individual. Individualized care is optimal care.
You are very fortunate that you are now seeing a MPN Specialist. This is the best way to ensure optimal MPN care. I expect the reassurance from this doc is on target and the best course of action is to just monitor and evaluate over the course of multiple labs.
Thank you, hunter5582. Your dissertation was very informative It is hard to wrap my head around being susceptible to hemorrhage as well as clotting. The information about the JAK+2 making the blood sticky was new to me. When I had the heart attack the nurse said my blood was very viscous but they did not know I had ET JAK+2 at the time. The platelets keep climbing since I first saw her 2 years ago so I guess I will have to wait for another 4 months because she is not requesting any earlier labs. Again, thank you, you have provided much insight
Normally this type of schedule is for when the patient is clearly stable on treatment and there is not a concern about the status of the ET. Given that your new doc is a MPN Specialist, perhaps a way to look at this is that it is reassuring that the doc does not think more frequent labs are needed.
Suggest that if you are concerned and do not want to wait, it is quite reasonable to ask the doc to order a CBC sooner than 4 months out. This is your prerogative as the patient. Most docs would not have an issue with ordering a CBC.
FYI - My platelet levels routinely cycled from the 500s to 700s for the better part of 30 years when I was not using cytoreduction. The platelet levels have gone up into the 900s when I was experiencing reactive thrombocytosis. I have never had a single incident of thrombosis. I have experienced some excessive hemorrhage and microvascular symptoms (erythromelalgia). These issues are now all very well controlled with aspirin and Besremi.
FYI - My former MPN Specialist (Dr. Spivak) explains it this way. Platelets are like little sponges. They soak up the von Willebrand Factor (needed for coagulation). When there are too many platelets, they soak up too much von Willebrand factor. That is, of course, a bit of an oversimplification but it is a good KISS explanation.
If you are interested in learning more about hemostasis (coagulation cascade) this is a great video. The video if not about MPNs per se, but provides a great explanation for how coagulation occurs. Note that hemostasis is very complex. Plan to make extensive use of the rewind button.
I always appreciate reading your clear explanations. Despite reading lots of info. I still find it hard to get my head round .you always give me a reminder of why as well as making sense .
It’s the contradiction s and of course how each individual responds to the same diagnosis.
The combination of conventional medics . Functional and gut feeling , instinct. For me Add up to understanding on best way to make decisions
That makes complete sense to me. We know that the MPNs are not monolithic disorders. There is a lot of variability in how the "same" disorder presents. I believe that the answer to why this is so lies in the genome. As we gain a deeper understanding of the underlying genetics we will better understand why the MPNs can present the ways that they do and individualize care to make it more effective.
Your decision making process certainly makes sense. Very similar to how I approach making decisions. In addition, add thorough research and understanding of the condition and all treatment options.
When I teach the self-advocacy sessions to young adults at Brainy Camp, it is based on three key principles.
Who knows your body best. "I do!"
What is your doctor not? "A mind reader."
Who is the Captain of your Care Team? "I am!"
These are the same principles I use in managing my own care. It works well for me.
I really like those 3 s advocacy phrases. I shall use them to help the kids I work with. Research is important , you and some others help those of us not possessed with the academic brain to understand ...
I'm CALR type 1 and also had a Heart attack on April 30th of this year. It started with chest pain then going to the emergency room where I had a slight T wave inversion and elevated troponin levels but D-Dimer normal. I was air lifted to a larger facility for a cardiac catheterization. The good news is that my cardiologist said " my veins and arteries are like a 25 year old, everything looked great" ( I'm 50 and exercise routinely) but none the less I had an event. My platelets at the time were 985 and he feels it was due to high platelets. Statistically having a thrombotic event particularly with CALR type 1 is low but none the less it happened. I made an appointment with my specialist but in the mean time I saw my local hemo where I was put on hydroxy Immediately. So a month later I met with my specialist and interestingly he thinks that my event was not a major vessel of the heart but rather a smaller vessel comparing it to a vascular event like visual disturbances or the tingling we get in our fingers. None the less it was enough to cause an event. My specialist agrees that statistically this should not have happened but my platelets are the smoking gun. In the end he Prescribed me Pegasys so I'm going down that path. Our goal is to get my platelets in-between 500 and 600. So in the end, sometimes we don't fit the stats and we just need to treat the patient, we are all very different in how we present. Sorry so long just saw some similarities.
Thank you, yes, similarities. Thank for sharing your story. It is encouraging to hear the back story to everyones’s diagnosis and knowing we are not alone in this journey
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It is hard to wrap my head around being susceptible to hemorrhage as well as clotting. The information about the JAK+2 making the blood sticky was new to me. When I had the heart attack the nurse said my blood was very viscous but they did not know I had ET JAK+2 at the time. The platelets keep climbing since I first saw her 2 years ago so I guess I will have to wait for another 4 months because she is not requesting any earlier labs. Again, thank you, you have provided much insight
Fellow ET Sufferers - increases platelet level whilst on Hydroxy
I have ET. Can increased stress, for instance due to a demanding work schedule, lead to an increased platelet count?
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