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Elastase Test?

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sunnyslumber

New Member
Hi,

Is there anyone here who's had Demeirleir's Elastase Test? Can you tell me some things like: whether he tests the concentration or the activity, what the reference range is, what your result was? I haven't had this test but I'd like to learn more about it, and I also wonder how much higher it is for us cfsers over the normal controls? To me Elastase is really interesting because it seems like an obvious potential way to connect the immune dysfunction theory people with the vascular damage theory people. Love to hear from you!


john
 

nickname

New Member
I have had the HLE (elastase) test done thru RED Labs in Belgium, which I believe, is the lab that DeMeirleir uses. I am however, not a patient of his. I live in the UK, and my husband ended up taking the blood over to them, because the blood is time sensitive, otherwise they can't use it.

The blood could have been made into a pellet and sent over on dry ice, but this is a big problem here, and labs are unwilling to do it. We could not find a UK lab who could do the HLE test either, so had to resort to RED. Look up their web site.

They report the value in U/mg extract - normal is less than 70 and mine was 131.

My consultant RX'd an oral beta lactam abx as per the latest DM research, because Cefobid, the drug DM used, is by jab only. I plan to start it this weekend, so cannot give you any feedback.

best wishes
nickname
[This Message was Edited on 04/06/2004]
 

sunnyslumber

New Member
Sorry to take so long to get back. I'm in college part time now and its taking a lot out of me. Sounds like a conservative estimate of the elastase dysfunction in cfs would be 2x upper limit of normal. That has to be doing Something... As you all probably know elastase is important in neutrophilic inflammation, and is considered to have a large role in the pathogenesis of cystic fibrosis (due to continuing neutrophilic inflammation in the lungs mostly, i think). I will definately try to think more on this when I get a chance. Btw does anyone know whether De Meirleir has decided to attribute the cleavage of RNaseL solely to either calpain or elastase yet? In the book this issue is unresolved.
 

nickname

New Member
If you have his book (and can understand it!!) would you tell me what he says about Actin - does this cause/contribute to RNaseL cleavage??

The elastase test that is done, tests the human leukocyte elastase, (HLE) which may well be differenct to the neutrophil elastase??

With thanks - nickname
 

sunnyslumber

New Member
I know after reading De Meirleir's book it seems things could never be this way, but I think you are making them too complicated ;). Leukocyte Elastase is a more general name than Neutrophil Elastase and refers to White Blood Cells (Lymphocytes, Neutrophils, Monocytes etc.). So it seems Neutrophil Elastase would constitute a subsection of Human Leukocyte Elastase as the name "Human Leukocyte" implies other immune cells are capable of producing elastase as well. It is my guess that these are two names for one identical molecule with the name corresponding to the origin of the Elastase, in HLE -any Leukocyte- and in NE Neutrophils specifically. It is my understanding that elastase is most strongly associated with Neutrophilic Inflammation so if that is correct then attempting to differentiate between the two names may be largely semantics.

Here is what I remember of the actin section (I'll try to reread it and go into more detail if you want though):
De Meirleir seemed to be arguing that a calcium dependent protease, m-calpain, was cleaving the capped form of actin (I don't remember the lines of evidence supporting this) causing the actin filaments to break down and releasing the DNA Binding Protein (otherwise bound to actin) which then enters the nucleus, binds DNA or something DNA related, enhancing the degradation of DNA and signalling the cell for apoptosis. Of course these "chewed up" actin filamints would be expected to decrease the cells mobility (its ability to home to a tissue and digest bacteria for example) and this process of actin degradation also releases actin fragments into the blood which it seemed from the context could serve as a marker for CFS and also cause hypercoagulation? I'm not sure about whether the degradation of action would itself enhance the loss of RNaseL, though if so it would probably be because the after effects (DNA Binding Protein etc)increase the expression of apoptotic enzymes which may cleave RNaseL... Even if this is so, I think it is (probably) a minor contributor to RNaseL loss, though my judgement is very likely based alot on the context of how it was treated in the book...

If you'd like my post in more accuracy and detail please tell me and I'll try to reread that section over the wkend.

Sincerely,


john
 

nickname

New Member
Many thanks for your reply. I have to agree, I am very guilty of making complicated things, even more complicated as a result of my not understanding!! But 24 hours after doing my post, and doing some googling, yes leukocyte and neutrophil elastase refer to the same thing, and always associated with inflammation.

If high elastase is therefore a result of inflammation, it can't be exclusively tied in with the RNaseL dysfunction seen in CFS (as I originally thought after reading the DM research) - it is seen in other diseases ie cystic fibrosis/lung diseases, other inflammatory diseases, and going back to your original post, vascular damage. Protease inhibitors can be used in all these diseases, so it would make sense to me to use them wherever elastase is high, regardless of any co-existing RNaseL dysfunction. Maybe high elastase found in CFS is a confirmation of its possible auto-immune component - maybe?

With ref to the actin, this is where I get really confused - if one has a positive LMWRNaseL, would it be possible to have a negative Actin, regardless of how the actin is cleaved?? I thought this would be impossible. Or am I being too complicated again??!!

Don't let me spoil your weekend, but would be grateful for your input, as and when you can.

With thanks
nickname


 
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