PPl with high hemaglobin/hematocrit what say you about this ?

[specter]

So this is very interresting..

 

[MyNameIsJeff]

Rex Feral and I discussed this issue at length in a previous thread. But that was before the new forum software, so the thread doesn't show up when using the search function...

In any case, the upshot is this: Elevated HCT due to erythrocytosis (or as it is more commonly referred to, secondary polycythemia) is not automatically harmless. There is such a thing as too high HCT, which is why phlebotomies in secondary polycythemia due to causes other than AAS are common practice. There is a debate about how high is too high. Some doctors say above 50, some above 52, some above 54, some above 60. Based on my review of the literature, I would start being concerned above 52, and act decisively above 54.

Some additional reading:

The development of secondary erythrocytosis in response to tissue hypoxia is physiologic and probably beneficial to many patients. The expanded red blood cell mass may partially or totally compensate for the lack of oxygen delivery and result in tissue oxygenation to its normal level.

At hematocrit levels higher than 60-65%, however, the compensatory increase in red blood cells reaches the limit of benefit and begins to compromise circulation because of hyperviscosity. The latter leads to greater tissue hypoxia and erythropoietin secretion, a continued increase in red blood cells, and further impairment of circulation.

To restore viscosity and maintain circulation at its optimal level, phlebotomize or remove the offending red blood cells. Some patients with extreme secondary polycythemia have impaired alertness, dizziness, headaches, and compromised exercise tolerance. They may also be at increased risk for thrombosis, strokes, myocardial infarction, and deep venous thrombosis. These are the patients who require phlebotomy.


The optimal level of hematocrit is one that is as close as possible to normal without impairing the compensatory benefit of increased oxygen delivery. This may be determined individually by symptom relief or decompensation, depending on the viscosity level.

Secondary Polycythemia Treatment & Management: Medical Care, Surgical Care

The word polycythemia indicates increased red blood cells, white blood cells, and platelets. Most of the time, it is used in place of erythrocythemia, or pure red blood cell increase, such as in secondary polycythemia.

emedicine.medscape.com

There is little evidence to guide management of congenital secondary polycythemia. Phlebotomy or venesection may be of benefit, particularly in patients at increased risk of thrombosis. A target hematocrit (Hct) of 50% may be the most practical. In patients with no specific contraindication, low-dose aspirin may be of benefit. In acquired cases of secondary polycythemia, management is based on treating the underlying condition.

Serious Cardiovascular Events and Clinical Outcomes in Secondary Polycythemia: Efficacy of Conventional Phlebotomy and Proposed Hematocrit Target

Abstract. Background: Recommendations for phlebotomy to treat erythrocytosis of Secondary Polycythemia (SP) are largely reactive and based on limited evidence a

ashpublications.org

Historically, phlebotomy has been used for the treatment of secondary polycythaemia in patients with chronic obstructive pulmonary disease. It results in an improvement of cerebral perfusion as well as sensory and mental function by lowering blood viscosity

Current applications of therapeutic phlebotomy

.

A 67-year-old man with polycythemia, secondary to chronic obstructive pulmonary disease, had angina attacks at rest treated successfully by supplementing conventional therapy with frequent phlebotomies. Although phlebotomy reduces arterial oxygen content, it also decreases blood viscosity, improves peripheral oxygen consumption and thus yields the clinical benefit.

Effects of phlebotomy on a patient with secondary polycythemia and angina pectoris

A 67-year-old man with polycythemia, secondary to chronic obstructive pulmonary disease, had angina attacks at rest treated successfully by supplement…

www.sciencedirect.com

Background: Recommendations for phlebotomy to treat erythrocytosis of Secondary Polycythemia (SP) are largely reactive and based on limited evidence acknowledging quality of life (QOL) metrics and thrombotic risk over Hct >54%. Unlike the large prospective polycythemia vera study (CYTO-PV), most data with erythrocytosis of SP derive from small retrospective studies and case series. We attempt to evaluate the association of pre-existing cardiovascular (CV) risk factors and Charlson Comorbidity Index (CCI) to determine outcomes with phlebotomy and create therapeutic cut-points to facilitate avoiding serious cardiovascular complications including DVT, pulmonary embolism, myocardial infarction, and cerebrovascular events.

Methods: A retrospective review of 143 patients with secondary polycythemia was conducted between December 2003 and March 2017. Patient demographics and outcomes after therapy were evaluated. CCI was used assess CV morbidity burden (low risk ≤4 vs high risk >4). The outcomes were defined as major events (DVT, PE, MI, CVA, PVD) and QOL symptoms or non-fatal events (headache, fatigue, and shortness of breath). The analysis included chi square or Fisher exact analyses where appropriate to identify associations. The protocol, and subsequent modifications, were reviewed and approved by the IRB at Texas Tech University Health Sciences Center.

Results: Our study evaluated 143 patients with a median follow-up of 46.8 months. The mean age of at diagnosis was 56.9 + 13.6y, and 71.3% were males. The most common etiologies were hypoxic Lung disease (COPD) 53.9%, obstructive sleep apnea (OSA) 33.6 % and testosterone use 6.9%. The mean Hct at diagnosis for the cohort was 52.3 + 3.3, the mean hematocrit after phlebotomy was 50.1+2.9. Achieving a Hct ≤ 52% during phlebotomy treatments was identified as low-risk group 40/143 (28%) vs Hct > 52% a high-risk group 103/143 (72%). Major CV events were recorded in 12.6% (13/103) patients in the low-hematocrit group and vs 37.5% (15/40) patients in the high-hematocrit group χ² (1, N=143) = 11.3, (p <0.001) Non-fatal/QOL events were recorded in 44.6% (46/103) of low Hct group and 62.5% (25/40) χ² (1, N=143) = 3.6, (p=0.055) of high Hct group. There was no association between QOL symptoms and major events χ² (1, N=143) =0.64, (p=0.423). A CCI >4 was associated with higher risk of major events in 50.0% (13/26) vs 12.8% (15/117) in the low CCI (≤4) χ² (1, N=143) =18.6, (p=0.0001). There was no association among non-fatal/QOL events and high 46.2% (12/26) or low CCI 50.4% (59/117) χ² (1, N=143) =0.155, (p=0.693). Use of ASA 325 mg daily was associated with decreased major events among aspirin users (6.6% vs 28.9%)χ² (1, N=143) =10.9, (p=0.001). There was no association between use of aspirin and non-fatal/QOL events. χ² (1, N=143) =0.56, (p=0.454).

Conclusion: Our cohort identifies a high-risk group with hematocrit of > 52 and a CCI > 4 that has significantly higher rates of serious CV events. ASA use was associated with decreased major events. The lack of relationship between QOL symptoms, Hct, major events, and CCI demonstrates a limitation in QOL symptoms to guide phlebotomy indication. Prospective studies are need to corroborate these findings.

Serious Cardiovascular Events and Clinical Outcomes in Secondary Polycythemia: Efficacy of Conventional Phlebotomy and Proposed Hematocrit Target

Abstract. Background: Recommendations for phlebotomy to treat erythrocytosis of Secondary Polycythemia (SP) are largely reactive and based on limited evidence a

ashpublications.org

 

[Matsuo Munefusa]

Rex Feral and I discussed this issue at length in a previous thread. But that was before the new forum software, so the thread doesn't show up when using the search function...

In any case, the upshot is this: Elevated HCT due to erythrocytosis (or as it is more commonly referred to, secondary polycythemia) is not automatically harmless. There is such a thing as too high HCT, which is why phlebotomies in secondary polycythemia due to causes other than AAS are common practice. There is a debate about how high is too high. Some doctors say above 50, some above 52, some above 54, some above 60. Based on my review of the literature, I would start being concerned above 52, and act decisively above 54.

Some additional reading:

Secondary Polycythemia Treatment & Management: Medical Care, Surgical Care

The word polycythemia indicates increased red blood cells, white blood cells, and platelets. Most of the time, it is used in place of erythrocythemia, or pure red blood cell increase, such as in secondary polycythemia.

emedicine.medscape.com

Serious Cardiovascular Events and Clinical Outcomes in Secondary Polycythemia: Efficacy of Conventional Phlebotomy and Proposed Hematocrit Target

Abstract. Background: Recommendations for phlebotomy to treat erythrocytosis of Secondary Polycythemia (SP) are largely reactive and based on limited evidence a

ashpublications.org

Current applications of therapeutic phlebotomy

.

Effects of phlebotomy on a patient with secondary polycythemia and angina pectoris

A 67-year-old man with polycythemia, secondary to chronic obstructive pulmonary disease, had angina attacks at rest treated successfully by supplement…

www.sciencedirect.com

Serious Cardiovascular Events and Clinical Outcomes in Secondary Polycythemia: Efficacy of Conventional Phlebotomy and Proposed Hematocrit Target

Abstract. Background: Recommendations for phlebotomy to treat erythrocytosis of Secondary Polycythemia (SP) are largely reactive and based on limited evidence a

ashpublications.org

Thanks for that. Any thoughts on the reasoning behind European doctors being more comfortable with higher HCT than American doctors?

 

[MyNameIsJeff]

Thanks for that. Any thoughts on the reasoning behind European doctors being more comfortable with higher HCT than American doctors?

There's an element of group think. We don't have enough evidence to say with certainty what the maximum acceptable HCT level is, only that it's somewhere in the range of 50 to 60. Some doctors rely more on study A, others more on study B. Some just do whatever their colleagues do or local (EU vs US) medical associations recommend. Some are too retarded or lazy to look it up and just make blanket statements like the guy in the video above.

 

[Matsuo Munefusa]

I've personally felt fine at 52-54 for years so I'm not scared when my HCT comes back "abnormal" there.

 

[Bio]

I would recommend anyone who is involved with AAS get tested to see if there are any genetic markers for clotting disorders. This would make a huge difference in how one approaches this!

 

[NEMSZ]

I would recommend anyone who is involved with AAS get tested to see if there are any genetic markers for clotting disorders. This would make a huge difference in how one approaches this!

I posted in another thread about clotting tests and they’re generally expensive like $500+.. I found the tests for something around $350 through Quest and got them tested and posted about it.. Needless to say it was one of the threads that got the least attention lol people want to spend $350-$500 on gear not health lol...

 

[Bio]

I posted in another thread about clotting tests and they’re generally expensive like $500+.. I found the tests for something around $350 through Quest and got them tested and posted about it.. Needless to say it was one of the threads that got the least attention lol people want to spend $350-$500 on gear not health lol...

I agree, people will spend a bunch on gear but let blood work and other tests fall by the wayside. $350 is money well spent when it could mean someone's mortality.

You should put a link from that thread in this one!

 

[nothuman]

I can chime in with my anecdotal experience.

I've spent considerable time with a hematocrit of 60 and hemoglobin of 20. Had I not tested, I would not have had any idea. This is despite copious blood donations over the years, giving me problematic ferritin and iron issues.

Other relevant points in my case when it comes to clotting/cardiac issues that would normally be connected to polycythemia vera (blood disease)
- My blood pressure was never elevated. Neither was heart rate.
- Platelets usually not much more than 200-250
- Fibrinogen normal
- MPO normal
- no sleep apnea
- no clotting factors such as Factor V, Jak2, etc.

The biggest symptom I've had from that is paranoia from knowing how high the numbers are. Fortunately, the numbers have come down since to 56/18.5 so I'm a little more comfortable with that.

Although it would be nice to lower those numbers even more, blood donations are absolutely NOT the answer for many of us. They only make the numbers come back even higher in my case.

 

[nothuman]

I also think PPI's are a terrible idea for 99% of people long term. You don't want to reduce NO (nitric oxide) production under any circumstances, let alone suppress stomach acid, which seems like a good way to speed aging since HCL deficiency is rampant, especially as we get older.

 

[maldorf]

I was taking a PPI for my esosinophilic esophagitis and it gave me crippling muscle cramps. I did not know why I was having them and after the 3rd time I had my wife drive me to the er because the pain was so bad and it would not abate. They ran all kinda of tests and couldn't find a anything wrong. I was concerned about electrolytes being off and affect on the heart, but levels were normal.

I told doctors I suspected the PPI, but they all told me its not a known side. Once I stopped the medicine, I never had it happen again. I switched to Pepcid. Prior to taking the PPI,I never had any either. It was only when I took the drug that it happened. Started in after taking it for about 2 weeks, and then reoccurred several more times over the subsequent 3 weeks.

Crippling cramps each time in the same muscle group while I was in deep sleep during the middle of the night. Being awakened by terrible cramps in my leg adductor muscles. Like a "Charlie horse" in my groin that lasted almost an hour.

Thats why I stopped taking PPIs.

 

[specter]

So the ppi should have been ppl meaning people my mistake

 

[NEMSZ]

I agree, people will spend a bunch on gear but let blood work and other tests fall by the wayside. $350 is money well spent when it could mean someone's mortality.

You should put a link from that thread in this one!

Heres the links to the website to order the blood tests;

Lab Testing API : Affordable Blood Testing | Lab Tests in US

Lab Testing API covers a broad range of Lab Testing Solutions. Our health team cares for your health and wealth with Affordable Lab Tests. Get in touch with us!

www.labtestingapi.com

They have Factor V as well and many others, just search on the site..

 

[GettingBackIn]

how are you handling this if not through blood donations? My story is very similar. I’m in my 40s. Only used gear a couple years after the army. I’m diagnosed with PV but my doc says my cells look normal, he just doesn’t have any other explanation. I get drained by prescription every 60 days. My numbers are now the same as yours 56/18.5

I can chime in with my anecdotal experience.

I've spent considerable time with a hematocrit of 60 and hemoglobin of 20. Had I not tested, I would not have had any idea. This is despite copious blood donations over the years, giving me problematic ferritin and iron issues.

Other relevant points in my case when it comes to clotting/cardiac issues that would normally be connected to polycythemia vera (blood disease)
- My blood pressure was never elevated. Neither was heart rate.
- Platelets usually not much more than 200-250
- Fibrinogen normal
- MPO normal
- no sleep apnea
- no clotting factors such as Factor V, Jak2, etc.

The biggest symptom I've had from that is paranoia from knowing how high the numbers are. Fortunately, the numbers have come down since to 56/18.5 so I'm a little more comfortable with that.

Although it would be nice to lower those numbers even more, blood donations are absolutely NOT the answer for many of us. They only make the numbers come back even higher in my case.

 

[nothuman]

I was taking a PPI for my esosinophilic esophagitis and it gave me crippling muscle cramps. I did not know why I was having them and after the 3rd time I had my wife drive me to the er because the pain was so bad and it would not abate. They ran all kinda of tests and couldn't find a anything wrong. I was concerned about electrolytes being off and affect on the heart, but levels were normal.

I told doctors I suspected the PPI, but they all told me its not a known side. Once I stopped the medicine, I never had it happen again. I switched to Pepcid. Prior to taking the PPI,I never had any either. It was only when I took the drug that it happened. Started in after taking it for about 2 weeks, and then reoccurred several more times over the subsequent 3 weeks.

Crippling cramps each time in the same muscle group while I was in deep sleep during the middle of the night. Being awakened by terrible cramps in my leg adductor muscles. Like a "Charlie horse" in my groin that lasted almost an hour.

Thats why I stopped taking PPIs.

PPI's would be a really bad idea in your case since they reduce NO production, which is paramount to proper heart function. Thank goodness you stopped

 

[nothuman]

how are you handling this if not through blood donations? My story is very similar. I’m in my 40s. Only used gear a couple years after the army. I’m diagnosed with PV but my doc says my cells look normal, he just doesn’t have any other explanation. I get drained by prescription every 60 days. My numbers are now the same as yours 56/18.5

I settled in on a dose of 15mg of test daily (105mg weekly) and it eventually went down over time without donating. Your doctor incorrectly diagnosed you with PV because he is either an absolute buffoon or hasn't been trained properly, assuming you told him you were on TRT.

 

[GettingBackIn]

I settled in on a dose of 15mg of test daily (105mg weekly) and it eventually went down over time without donating. Your doctor incorrectly diagnosed you with PV because he is either an absolute buffoon or hasn't been trained properly, assuming you told him you were on TRT.

I was off of all test for a year without my levels lowering at all (60/22). A few donations in a row got me down to where I am. Is there another condition other than PV anyone knows of that I should ask about? Could a few years of moderate use cause levels to elevate permanently without PV or another disorder?

 

[maldorf]

I was off of all test for a year without my levels lowering at all (60/22). A few donations in a row got me down to where I am. Is there another condition other than PV anyone knows of that I should ask about? Could a few years of moderate use cause levels to elevate permanently without PV or another disorder?

My hematologist did a bone biopsy to test me. Its a simple procedure done right there at the office. They just stick a needle into your hip bone and pull a small plug out. Doesnt hurt at all. The biopsy will help rule out serious trouble. Mine was normal. For me, just doing hrt raises it.

 

[Itachi]

I was taking a PPI for my esosinophilic esophagitis and it gave me crippling muscle cramps. I did not know why I was having them and after the 3rd time I had my wife drive me to the er because the pain was so bad and it would not abate. They ran all kinda of tests and couldn't find a anything wrong. I was concerned about electrolytes being off and affect on the heart, but levels were normal.

I told doctors I suspected the PPI, but they all told me its not a known side. Once I stopped the medicine, I never had it happen again. I switched to Pepcid. Prior to taking the PPI,I never had any either. It was only when I took the drug that it happened. Started in after taking it for about 2 weeks, and then reoccurred several more times over the subsequent 3 weeks.

Crippling cramps each time in the same muscle group while I was in deep sleep during the middle of the night. Being awakened by terrible cramps in my leg adductor muscles. Like a "Charlie horse" in my groin that lasted almost an hour.

Thats why I stopped taking PPIs.

Omeprazole gave me this side effect. I was cramping in my triceps and lats which I've never had happen to me in over 10 years of lifting weights. Other places yeah, those places, never. Discontinued and they went away.

Oddly enough I'm having the opposite problem of what this thread is about and I believe it's related to long term PPI use. My hematocrit hasn't budged in several years and I've been using high dosages of anabolics almost year round. PPI's seem to have made me anemic and it's keeping my RBC low. My hemoglobin used to get up to 19 or 20 on cycles.

 

[Starchild1]

My HCT is always around 54-56 regardless. Everything else is fine and no clotting factors so I have come to accept this as just the way things are. I have zero sides from it, so I'm no longer letting it stress me out. I think the stress and worry would be more troublesome in my case lol.