Anyone else find the side effects of Hydrea 500MG frightening?

Hi @garyr443 Just wondering, Is there any reason you can’t still take the cranberry juice daily even though you’re back on the HU and the BP med? I ran a drug interaction and there aren’t any contraindications between cranberry, lisinopril and HU.

The anti-inflammatory properties of the unsweetened cranberry juice were certainly noticed by you over the month with less pain and an increase in balance and coordination. Not sure why you can’t have some in moderation. I drink unsweetened Monterey cherry juice daily. (1 ounce Concentrated juice gets mixed with 8 oz water). I think it would be similar in properties as your cran juice. Just a thought…

@loribmt Thank you, Lori! I couldn't have asked for a more complete explanation. About the juice bust, I figure I was up against something much more complex than Type 2 Diabetes, and what you've written here certainly confirms that's the case. Ah, but there were some things about the cranberry juice that I really did enjoy (no, not so much the flavor!), such as a moderating effect on body pain, especially in my feet, and I noticed an increase in my balance and coordination. I sure missed all this today when I was out doing photography!

Dear susi . . . with a platelet count in the 900s, OF COURSE you have headaches and are exhausted! Those are the two most widely-experienced symptoms of ET itself.

I hope that as HU brings down your count, you will start feeling much better!

Hang in there!

Hello, susi1950.

HU slows production of platelets. It does not destroy them. As far as I know, at this time, there is no medication that destroys platelets.

Here's a quick Google AI summary of information provided by the National Institutes of Health.

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Hydroxyurea (HU) is the standard first-line therapy for high-risk essential thrombocythemia (ET) patients. It lowers platelet counts to safer levels, actively reduces the risk of life-threatening blood clots (thrombosis), and decreases the size of mutated cell clones (such as JAK2) in the blood.

Here is exactly how hydroxyurea helps patients manage ET:

Normalizing Platelet Counts: ET is characterized by an overproduction of platelets. HU targets rapidly dividing cells in the bone marrow, slowing down the production of blood cells and preventing platelet levels from reaching dangerous, clot-inducing heights.

Preventing Thrombosis: By controlling platelet counts, HU significantly lowers the rates of cardiovascular and thrombotic events, such as heart attacks and strokes, improving overall survival in older patients.

Treating Specific High-Risk Groups: It is the guideline-recommended frontline therapy for patients over 60 or those with a prior history of thrombosis. It can also be prescribed for younger patients facing persistently high platelet counts.

Reducing Driver Mutations: Clinical trials show that HU can successfully reduce the burden of mutated cells (like the JAK2V617F mutation), helping target the underlying genetic drivers of the disease.

@garyr443 my ET is caused by the same mutation-CALR 9- that you have. My doctor said I was born with it. It just activated when I hit 73. Mutations are weird like that! I started with 1000mgs HU once a day. That was in April. My platelets dropped like a stone! They are now at 256 from 867. My red blood cells have also dropped big time. My white are just hovering above the “too low” level. My CNP lowered my dose to 500mgs once a day, but last blood test showed the platelets still at 256 and a continued fall of my red blood cells. I have an appointment soon and will see what the doctor thinks. I was utterly exhausted before the HU was lowered. The skin under my nails is dark grey to black. I wear nail polish to cover that up! I still feel tired each day, but it isn’t so bad now. I never nap! I eat like I always have and exercise a lot. Everyone is different, so you kind of have to decide what your goal is and how to reach it. You probably don’t want to have a stroke or heart attack from a clot, so that should weigh in as you decide your path forward. There are other drugs besides HU. ET is not well researched yet, so the older drugs used to treat the condition successfully are the ones the doctors like to prescribe. Still, all the feedback on these treatments has to come from us, the patients. So, speak up else how will our doctors know what this is like! I speak up a lot!

@janemc The cause is an acquired mutation, though which mutation it is seems to vary. Mine is the CALR Exon 9 mutation and, apparently, it has existed since I was 52, as that's when an old medical record shows my platelet count was first recorded as being high. The year before, it was normal. I'd like to learn more about these mutations and just how and why they are "aquired," but there doesn't seem to be any information about this.

@1pearl

I'm so glad you're doing great!

This is yet another example of why an ET diagnosis is so diabolical.

I hear one thing from my oncologist . . . others hear something else entirely.

Utterly confusing.

To me, what I heard makes sense: manic overproduction of platelets strains bone marrow. With HU, the stress on the bone marrow is reduced.

Without intervention, the bone marrow is depleted. And the success of a bone marrow transplant is far from assured.

How long will it be before MPNs are truly understood? Not in my lifetime, I'll bet.

Hi @garyr443. Every second, our bone marrow produces several million blood cells. Over a single day, we produce 200 billion red blood cells, 400 billion platelets, and 10 billion white blood cells. Each cell replicating with incredible precision, identical clones of each other. It makes a copy of its DNA and sometimes the copy is not quite perfect. That small difference from the original DNA sequence is a mutation. All it takes is one strand of DNA to misfire in a cell to set the ball rolling for a blood cancer or condition.

We all have cancer cells floating around our body daily. But our immune system is on a mission to seek and destroy these rouge cells. Some of the defects that happen also allow them to go undetected by our immune system. When that happens, those defective cells keep proliferating without an off switch.

Most of the defects have unknown causes as to what triggers the misfire, but there are some strands of DNA more susceptible to mutation than others. From what I learned mutations can happen randomly. There are spontaneous mutations that concur naturally during DNA replication without any external influence. And some through exposures to toxins such as pollution, viral infections which can insert their genetic material into host DNA, causing mutations, ionizing radiation found naturally in our environment, from random gamma rays shooting through the earth, the aging process, etc., all of which may break down healthy DNA. If there’s a weak spot, that’s the first place to misfire.

In your case, you have acquired a mutation on your CALR gene. Mutations on that gene change the protein in a very specific way. They alter the last section of the calreticulin protein, called the C-terminus, the tail end of the protein chain. Every time a cell with that defective DNA splits it creates malignant clones.

The good news is that with continued research, there are new abrogating drugs and targeted therapies being developed which are aimed at molecular remission and eliminating the malignant clones.
I’ve benefited from abrogating drugs myself in my AML (acute myeloid leukemia) odyssey. I have some amazingly brilliant research scientists on my medical team. We’ve discussed my case at length. While there may be theories as to what caused my 3 mutations of AML, there was no precipitating event that could be attributed. But thanks to these targeted drugs, the most aggressive mutation was curtailed.

So the good news for you and others with the CALR mutation is that there are ongoing clinical trials for bispecific antibodies. These are engineered to bind to the mutant CALR while simultaneously engaging a T-cell to destroy the malignant clone.

In fact, right now, our own member @drbart86 is involved in this clinical trial for the CALR mutation! He’s been sharing his journey with us.
https://connect.mayoclinic.org/comment/1607218/
Other areas being explored are:
~Chimeric Antigen Receptor (CAR) T-cell therapy
~Peptide vaccines to train the patient’s immune cells to eliminate cells carrying the CALR
mutation is another area of potential.

While you may never know the exact cause of your mutation there is hope on the horizon that you may not always need the HU. I’m sorry to see the juice experiment was a bust. But thank you for sharing your information with us.