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Catecholamine Levels


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Does anyone know what your supine and standing NE levels are supose to look like for POTS. I got a copy of all my blood work from VANDY and mine do not seem consistant with POTS or at least the hyper form of POTS. My supine level was 88pg/ml and standing was 386 pg/ml.

THANKS!!!!

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Does anyone know what your supine and standing NE levels are supose to look like for POTS. I got a copy of all my blood work from VANDY and mine do not seem consistant with POTS or at least the hyper form of POTS. My supine level was 88pg/ml and standing was 386 pg/ml.

THANKS!!!!

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/

For some on Vanderbilt's current studies on POTS, an inclusion criteria is a NE > 600 pg/ml. The article I pasted above states the "hyperadrenergic" group often has levels > 1000 pg/ml. So, by this definition, you would not have the hyper sub-type. I have no idea what levels are in the normal population.

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Does anyone know what your supine and standing NE levels are supose to look like for POTS. I got a copy of all my blood work from VANDY and mine do not seem consistant with POTS or at least the hyper form of POTS. My supine level was 88pg/ml and standing was 386 pg/ml.

THANKS!!!!

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501099/

For some on Vanderbilt's current studies on POTS, an inclusion criteria is a NE > 600 pg/ml. The article I pasted above states the "hyperadrenergic" group often has levels > 1000 pg/ml. So, by this definition, you would not have the hyper sub-type. I have no idea what levels are in the normal population.

Thank you for the response, that was a helpful article. I guess I can rule out the hyper version. The Doctor that wrote that article is one of the ones I saw at Vanderbilt. At the time I went there was no inclusion criteria for NE level. Their main inclusion criteria at that time was heart rate increase >30 BPM. Are they now requiring the >600 pg/ml for a POTS diagnosis or just for their current studies?

The more I try to understand about this condition the more I realize I have to learn. There is a lot of medical terms used on this board that I am trying to understand better. It seems for every medical post I read I end up having to look up several terms. In order to understand those terms I have to look up more terms. Anyway I was trying to understand and rule out "hyperandrenergic" pots and now I can.

Thanks

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The catecholamine level is definitely not a requirement for a POTS diagnosis. It is just an inclusion criteria for some of the recent POTS studies at Vanderbilt, not a diagnosis. I venture to guess that these levels vary from day to day in POTS patients anyway.

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The catecholamine level is definitely not a requirement for a POTS diagnosis. It is just an inclusion criteria for some of the recent POTS studies at Vanderbilt, not a diagnosis. I venture to guess that these levels vary from day to day in POTS patients anyway.

That is what I thought but was not sure.

Thanks!

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Most research bodies do not include catecholamine levels as a requirement for diagnosis of POTS.

The term hyperadrenergic POTS as a definition of a sub group of POTS patients is not universally accepted by all research groups; Some research suggests the levels of catecholamines present may just relate to beta 2 receptor genetics or as Mayo recently described it - as an secondary feature to one underlying problem which they currently believe is autoimmune disruption of a3 acetylcholine receptors.

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Or just the bodies natural, healthy compensatory mechanism to getting blood to the brain and other critical organs when blood is pooling down south?

I agree, I like that explanation because I can actually understand it. I was looking further at my blood work this AM and found on one occasion my NE did rise on standing to 893 from 138 (they took so much blood from me I am suprised I had any left). That was the baseline for the saline study so it was a fairly benign test. You were right when you said that you NE reaction can vary.

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Or just the bodies natural compensatory mechanism to getting blood to the brain and other critical organs when blood is pooling down south?

I'm in agreement with this theory. My NE levels upon standing were 1089, and my local cardio thought I'd benefit from clonidine. I couldn't even tolerate 1/8th of the normally prescribed dose without my BP plummeting (and it normally rises with upright posture). So yes, in my case the elevated NE levels were a healthy, compensatory reaction to pooling.

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Or just the bodies natural compensatory mechanism to getting blood to the brain and other critical organs when blood is pooling down south?

I'm in agreement with this theory. My NE levels upon standing were 1089, and my local cardio thought I'd benefit from clonidine. I couldn't even tolerate 1/8th of the normally prescribed dose without my BP plummeting (and it normally rises with upright posture). So yes, in my case the elevated NE levels were a healthy, compensatory reaction to pooling.

I am on the tail end of 10-day trial and taper off of the clonidine. Prior to clonidine, My blood pressure had been running high when upright, and I was experiencing the adrenaline surges many of us are so familiar with. I noticed the clonidine took away the symptoms of the adrenaline surges, but my primary orthostatic symptoms (headaches, coat hanger pain, brain fog, dizziness, and fatigue) were worse. I'm feeling better now that I am off, but I'm glad that I gave it a go. I know clonidine benefits many POTS patients, but it wasn't for me either. My new plan is to hit the gym and rowing machine to try to strengthen my heart to maximum capacity. I do pretty well with exercise, but the sitting or standing without aerobic activity is torture. I am grateful for the Florinef and DDAVP, but the other medications have been a bust, so on to more non-pharmacological methods.

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The theory behind most POTS patients is that parts of the vasculature are less sensitive to norepinephrine than normal due to reduced receptor expression or neuropathy. So the body shoots off extra to get these areas to vasoconstrict correctly, but the parts of the body do not have reduced sensitivity, thus feel the extra norepinephrine such as the heart where adrenergic tachycardia results. So the extra levels required to get the reduced sensitivity areas to constrict causes symptoms of excess norepinephrine in other areas.

But its a natural mechanism to attempt to increase blood flow to the brain, although it can actually cause cerebral vasospasm and other problems that result in more problems.

In other forms of POTS the body is too sensitive to normal norepinephrine, the body does not take norepinephrine out of the synapse correctly, or the parasympathetic system effects cerebral autoregulation.

I guess my point is that its hard to say whether its a normal coping mechanism to deranged blood flow regulation or the primary problem at this stage.

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The theory behind most POTS patients is that parts of the vasculature are less sensitive to norepinephrine than normal due to reduced receptor expression or neuropathy. So the body shoots off extra to get these areas to vasoconstrict correctly, but the parts of the body do not have reduced sensitivity, thus feel the extra norepinephrine such as the heart where adrenergic tachycardia results. So the extra levels required to get the reduced sensitivity areas to constrict causes symptoms of excess norepinephrine in other areas.

But its a natural mechanism to attempt to increase blood flow to the brain, although it can actually cause cerebral vasospasm and other problems that result in more problems.

In other forms of POTS the body is too sensitive to normal norepinephrine, the body does not take norepinephrine out of the synapse correctly, or the parasympathetic system effects cerebral autoregulation.

I guess my point is that its hard to say whether its a normal coping mechanism to deranged blood flow regulation or the primary problem at this stage.

That makes sense. What is a cerebral vasospasm? Is this something that could be causing my massive brain fog?

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The theory behind most POTS patients is that parts of the vasculature are less sensitive to norepinephrine than normal due to reduced receptor expression or neuropathy. So the body shoots off extra to get these areas to vasoconstrict correctly, but the parts of the body do not have reduced sensitivity, thus feel the extra norepinephrine such as the heart where adrenergic tachycardia results. So the extra levels required to get the reduced sensitivity areas to constrict causes symptoms of excess norepinephrine in other areas.

But its a natural mechanism to attempt to increase blood flow to the brain, although it can actually cause cerebral vasospasm and other problems that result in more problems.

In other forms of POTS the body is too sensitive to normal norepinephrine, the body does not take norepinephrine out of the synapse correctly, or the parasympathetic system effects cerebral autoregulation.

I guess my point is that its hard to say whether its a normal coping mechanism to deranged blood flow regulation or the primary problem at this stage.

Could you also give me a laymans explanation for cerebral auto regulation? I try to look these terms up myself but just end up with more questions.

Thanks.

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