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» LymeNet Flash » Questions and Discussion » Medical Questions » TNF(tumor necrosis factor) and Cox-2 inhibitors

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Author Topic: TNF(tumor necrosis factor) and Cox-2 inhibitors
Kendrick
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I noticed my TNF was high on blood tests... and after looking at it more, it seems to be a cytokine that causes inflammation, and some neurological issues.

It is common in RA, Lyme, and other autoimmune diseases. I also read where issues with inner ear inflammation has been shown to have increased TNF in the ear.

I was looking at many websites(wish I had them for you now), but generally the treatment is COX-2 inhibitors such as Celebrex.

I was wondering if anyone had any experience with a COX-2 inhibitor helping them while being treated?
The doctors can not figure out why I am dizzy and off-balanced after Inner ear tests and Brain MRI.

--------------------
Never walk through a cornfield backwards.

About me(Yahoo): http://360.yahoo.com/profile-NR1Y8cw6fqhtrewwItSlfsgQDIhaOojd

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AGuess
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Several years ago, before I found out that I had Lyme and Babesia, I was told that I had RA.

I had sudden onset swelling of my left hand, which became a claw, then moved to my shoulder, then to other hand. My neck was stiff and then I got where I could not walk due to pain in the bottom of my feet.

First I was told I had Parvo virus, then RA.

Vioxx, a cox-2 inhibitor really helped, and I also did many different RA treatments with Enbrel being the most helpful. This lowers the TNF.

However, after finding out I had Lyme, and doing about 5 months of treatment, I was able to end the Enbrel treatments.

I now manage any type of joint pain with minocycline and lodine.

AGuess

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Lymetoo
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quote:
Originally posted by Kendrick:


The doctors can not figure out why I am dizzy and off-balanced after Inner ear tests and Brain MRI.

Couldn't that be from the Lyme?? Have you been diagnosed yet?

--------------------
--Lymetutu--
Opinions, not medical advice!

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Kendrick
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Yes, maybe from Lyme, but to take it a step further. Why does Lyme cause dizzyness?

Lyme causes increase in TNF... is this possibly the cause?

If so, maybe COX-2 inhibitors could possibly help(while being treated)?

--------------------
Never walk through a cornfield backwards.

About me(Yahoo): http://360.yahoo.com/profile-NR1Y8cw6fqhtrewwItSlfsgQDIhaOojd

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summerlove
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kendrick,
I sent you a pm.

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Kendrick
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Thank you... has anyone tried this for dizzyness, light-headedness?

--------------------
Never walk through a cornfield backwards.

About me(Yahoo): http://360.yahoo.com/profile-NR1Y8cw6fqhtrewwItSlfsgQDIhaOojd

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Nebula2005
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Dear Kendrick

My TNF was also elevated. Not terribly high, but above normal. I did some research on lowering it and found out it's not easily done.

Thus the development of Enbrel, Humira and other specific TNF blocking drugs.

With Lyme disease there are so many cytokines involved, TNF may not even be what's causing your symptoms.

I took Celebrex for arthritis but it didn't agree with me. I have drug metabolism issues.

It targets prostiglandins (sp?), as does ibuprofen. It's supposed to be easier on the stomach, as ibuprofen and other NSIDS like aspirin cause bleeding.

I have ear problems, too--I don't get dizzy, but I feel off balance and I have terrible pain and tinnitis. Also my ears twitch and flush bright red.

It may well be that Celebrex could help your symptoms. Lyme nerve involvement is probably the cause.

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Marnie
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While some inflammation is necessary, indeed too much is NOT GOOD.

But beware...this is tricky!!!

Humira "side effects" include cancer and TB.

TNF alpha and IL1 beta are up for many reasons.

We look to be "stuck" in an "allergic" response to the antigens in Bb's cell wall.

When Bb enters the mitochondria of the cell, it triggers the nucleus of the cell to release an enzyme called NFkB. This looks to trigger TNF alpha which signals the beta cells...specifically the IL1 B cells.

Now...here are some "upsides" to TNF alpha (old file so some links might not work):

Benefits of TNF alpha:

1. ``as more people are treated with TNF inhibitors over longer periods of time, tumor risk may become more pronounced.''
(May protect us from tumors.)

www.Hopkins-arthritis.som.jhmi.edu/edu/acr2003/ra-treatments.html

2. ``TNF-alpha is potentially an important mediator of protein wasting in chronically uremic patients.''

www.dscmt.univ.trieste.it/text/curriculum/containerbiblio.htm

3. ``one mechanism of action of TNF-alpha ...on thyroid FRTL-5 cells is to inhibit calcium entry.''
PMID: 10092616

4. ``is actually a potent modulator of neurotransmitter interaction.''
hdlighthouse.org/see/immune/tnf.htm

5. ``the body does use tumor necrosis factor-alpha (TNF-alpha) to acutely fight infections. If patients
are showing any sign of infectious disease, drugs such as Enbrel (that inhibit the effects of TNF-alpha) are temporarily discontinued.''
www.lef.org/protocols/prtcl-128a.shtml

6. ``After noticing that exposure to the naturally occurring compound TNF-alpha (Tumor Necrosis
Factor-alpha) killed malfunctioning immune cells...''
www.diabetesincontrol.com/issue166/item1.shtml

7. ``generally the level of TNF increases with aging. Lactic acid and unsaturated fats and hypoxia
stimulate increased formation of TNF. Estrogen increases production of nitric oxide systemically, and nitric oxide can stimulate TNF formation. When oxygen and the correct nutrients are available, the hypermetabolism produced by TNF could be reparative (K. Fukushima, et al., 1999), rather than destructive.''
http://www.ferlowbrothers.com/estrogen_osteoporosis.htm
(Original website would not link. Above website says the same.)

8. ``TNF-a is a molecule responsible for activating and proliferating cells of the immune system as
well as protecting the body from abnormal cell growth.''
(same source as #7)

9. ``Activity of TNF-a is associated with inflammation, cytotoxicity (destruction of abnormal cells)
antiviral activity, and the proliferation of immune cells.''
(same source as #7)

10. ``modulate cell proliferation and cellular calcium homeostasis.'' http://www.cell-research.com/991/991-syf1.html

(If you go to the above website, please note the mention of spingolipid metabolites and keep this in mind: syhingomyelinase is Mg dependent)

PMID: 9195931

11. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody''
PMID: 12522038

12. ``The increased bone resorption may be due to an increase in TNF-alpha''
PMID: 14704297

13. ``no detrimental effects on normal neurons and can protect neurons when present in neuronal cultures during in vitro ischaemia...Once TNF's removed, neuroprotection is lost.''

www.anri.uwa.edu.au/teams/teamcvdl/cvdl.htm

14. ``TNF- a also causes production of sphingosine which can directly block the release of calcium
from the sarcoplasmic reticulum and therefore depress cardiac contraction.''

www.saem.org/download/01kline.pdf

15. ``suppression of insulin action in the liver resulting from TNF-alpha mediated suppression of
tyrosine phosphorylation''
Gastroenterology 2004; 126: 840-848,917-919
(Keep in mind insulin ACTIVATES PFK which Bb is dependent on.)

16. ``Total elimination of the TNF-a cytokine apparently creates a less hostile immune environment...Although `Chronic-lyme' is a lympopenic disease, chronic lyme patients do not usually form sarcoid granuloma. Borrelia burgdorferi appears to be a pathogen with insufficient lympopenic activity to proliferate sarcoid granulomas on its own. However, together with other pathogens, it is frequently found as a component of sarcoid inflammation.''
www.joimr.org/phorum/read.php?f=2&I=38&t=38

17. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody''
PMID: 12522038

18. ``Polymerase chain reaction analysis indicated a protection rate of 95% in mice receiving tumor
necrosis factor (TNF)-alpha.''
PMID: 8537658

19. These results are in line with previous experiments using cells of the adaptive immune response, indicating that strong T helper type 1 (Th1) proinflammatory responses might be associated with a
successful resolution
of Lyme disease.

PMID: 15958074

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Nebula2005
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So increasing TNF-a is just one more example of the immune system trying to fight and cope with the chronic infection?
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Marnie
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Yup. Because too many of our OWN antibodies are defective (fab portion).

The body has to find another route(s) to prolong our life.

In a relatively short time...it gets harder to REACH the infected cells which complicates the matter.

Interesting...

A Dr. Sinatra's suggested "cocktail" for CFS:

abreathofhope.blogspot.com/2005_11_01_abreathofhope_archive.html

Once we make more ATP, this should restore the Na-K pump and more ATP will also drive Mg back INTO the cells.

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northstar
Frequent Contributor (1K+ posts)
Member # 7911

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Marnie,
That is interesting. I had read somewhere that it
is best to take the acetyl -l-carnitine with
CoQ10, which I had done. This is the reason.

The Sinatra formula also adds d-ribose.

Think I will add that and read more about it.
I know you have brought that up
several times.

Interesting article about all the CF supplements.

Northstar

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