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Gliadin is a molecule that is a part of the larger gluten molecule. Deamidated
gliadin is gliadin partially broken down by tissue transglutaminases (tTG).
Gliadin is soluble in alcohol and deamidated gliadin is soluble in water. The
tests are for antibodies to these gliadin or deamidated gliadin molecules. The
original test is for antibodies to the intact gliadin molecule. The deamidated
test is for antibodies to a partially disassembled gliadin molecule . Because
antibodies bind to their target (gliadin) in a lock-and-key form, the "locks" on
gliadin are different than on deamidated gliadin. The research presented by Dr.
Alaedani at the Las Vegas NAF conference shows gliadin antibodies binding to the
brain protein synapsin. There does not appear to be any research that shows
deamidated gliadin antibodies bind to any proteins in the brain.
In short, original Gliadin IgG antibody test is the test for potential Gluten
Ataxia. The newer deamidated gliadin IgG antibody test is for Celiac Disease and
Celiac Disease (intestinal damage). Note, someone with Celiac Disease can also
have Gluten Ataxia but they can also have B1,B12, E Ataxia because of inadequate
absorption in the gut.
If you have recently had a gluten antibody test, you most likely have had the
Deamidated Gliadin Antibody test. For a person with Gluten Ataxia but not Celiac
Disease, the deamidated test will show a much lower or essentially zero value which
will likely result in a false negative result of "normal". If you suspect you have
Gluten Ataxia you must get the original (non-deamidated) Gliadin Antibody test.
You need to work with your doctor carefully to request the proper test and verify
with the local lab taking your blood that they are sending your sample to the
correct testing lab. See the following:
As of the current date (06/11/ 0 the only U.S. labs I know of offering the
correct Gluten Ataxia test are the following with reference ranges:
For Quest Diagnostics,the correct test: Code: 8889X or 3517N Gliadin Antibody Panel
Reference Ranges:
IgA NEGATIVE: less than 11 U/ml
IgG NEGATIVE: less than 11 U/ml
http://cas2.questdiagnostics.com/scripts/webdos.wls?MGWLPN=QDCIAP20&wlapp=DOS&OrderCode=3517N&SITE=4&SearchString=3517&tmradio=title
Your doctor needs to write the lab request to state specifically it must be done
by "Quest" and the specific test code "8889X" from above (or maybe "11212X"). The
doc should not say "non-deamidated" as the lab will not know what to do. Again,
if the request does not say something like "Gliadin Antibody by Quest - test code
8889X" you may end up running in circles for weeks to get it done right.
It looks like one could also substitute in the Quest Diagnostics test Code: 11212X
but this only tests IgG with the same reference ranges as above.
http://cas2.questdiagnostics.com/scripts/webdos.wls?MGWLPN=QDCIAP20&wlapp=DOS&OrderCode=11212X&SITE=4&SearchString=GLIADIN&tmradio=title
For Specialty Laboratories the correct test is:#1266: Gliadin IgG & IgA Antibodies.
But read the rest of this paragraph. Specialty Laboratories has been purchased by
Quest so this test will probably be phased out in 2008 or 2009. Specialty Labs
has a new test called the gliadin (MGP) Ab test. The MGP stands for modified
gliadin peptide which means this new test will be a deamidated test. Because of
this new test, I do not recommend Specialty Labs because they may very well convert
all gliadin Ab tests to the new one unless specifically specified by number.
-----------------------------------------------------------------------------------
The following labs only have the deamidated gliadin test which is the wrong one for
Gluten Ataxia.
For LabCorp, there appears to be no correct test left. All of their tests are
deamidated. If a test was taken prior to the deamidated test, the test may
have been correct but you must contact LabCorp to see when the switch occurred.
For reference the old test data follows:
the old test was: Number 163402 - Gliadin Antibody Profile, IgG,
IgA, EIA CPT 83516
Reference RAnges - Updated February 6 2007
IgA: Negative: 0-4 U/mL
IgG: Negative: 0-9 U/mL
http://www.labcorp.com/datasets/labcorp/html/chapter/mono/bs004000.htm
For ARUP Laboratories ALL GLIADIN TESTS ARE DEAMIDATED EVEN THOUGH THE DESCRIPTION
DOES NOT SAY SO! Mayo Clinic currently only lists deamidated gliadin tests.
If you get a test from another lab or information about one, let me know and I will
track it down and update it here.
Old-FAQ Bear
P.S. Make sure doc does not say "non-deamidated" on lab req - Thanks LindaS!
P.P.S. Edited for new slight change on test numbers 06/28/09
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Bear, I looked up microglia in Mosby's Medical Dictionary, (fourth edition) and it is there. There isn't a whole lot of information, but somebody up to snuff on their neuroanatomy should know about them. I suspect I knew about them but sort of forgot that I did. The suffix glia should have given me a clue. There are several types of glia cells. They are brain cells that are not neurons.
I would place a very big bet that anybody who got through medical school knows about microglia. I almost never "talk shop" with my doc relatives. None of them specialized in neurology or genetics, so this kind of talk would probably bore them to death.
Do you know if Dr. Aleadina did his research in vitro? I would suspect that he did because he is a chemist and they usually don't mess around with living things. I'm thinking about the blood brain barrier and if a gliadin anti-body can pass through it. An in vitro experiment would not have to deal with that problem. The blood brain barrier sort of sounds like the neutral zone between the Klingons (it might be the Romulans, I kind of think so) and the Federation, but really it is just the term to describe the relative impermeability of blood vessels in the nervous system so that only very select things can get through.
There are several reasons why the blood brain barrier can become more permeable and allows more things to pass from the bloodstream to the nervous system. Some of these reasons have to do with the microglia and are usually symptoms of something wrong with the nervous system. Could this maybe explain why some people with a certain level of anti-bodies do not have ataxia and some people with the same level do? Do you know of any research that has dealt with this issue? That has been the central question to me about gluten sensitivity ataxia for several years.
ATILLA
Mrs. ATILLA still loves me |
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ATILLA,
Perhaps later I will post a more detailed response in a new thread. I posted this
one because I was bumping it for someone and it disappeared - probably pilot error
but I now compose everything in a text editor so I have copies.
I think Mosby's is out of date. Wikipedia won major points in a face off against
Encyclopedia Britannica for that reason. The reviewers called it a tie with
Britannica being more accurate but dated and with much fewer topics covered.
Apparently glia cells are "sometimes" doing things somewhat like neurons. That
evolution thing again.
It would depend on when doctors went to med school. Microglia were discovered in
1880, studied in the 20's and then kind of ignored until 1988. It probably took
5-10 years to hit the medical textbooks. I think they are a hot area of research
now. Now about that bet that applies to "anybody who got through medical school"...
Armin Alaedini is not an MD and I think he has a PhD in Biochemistry. He is with
The Department of Neurology and Neuroscience at Cornell. He is working with doctors
so he gets blood samples from patients but his research would probably all be in
vitro. I have not carefully read all of his papers so I don't know if he also used
cerebrospinal fluid but it would have been available if needed. He also has access
to all the available research including autopsy evidence of gliadin antibodies in
the cerebellum of patients with positive blood tests and Ataxia.
Before talking about the blood brain barrier, there are a couple of misconceptions
that people keep falling into. I'll try to make a short summary that may have not
be totally correct in all situations. The lymphocytes are the cells involved in
autoimmunity (in general but there may be exceptions). When young lymphocytes are
maturing in the thymus or lymph nodes and their receptors encounter and STRONGLY
bind to their unique antigen, they are supposed to commit suicide or be inactivated.
The reason seems to be any antigen in the thymus or lymph nodes is likely to be a part
of the body (self-antigen). This process is called "central tolerance". If a person
is low on vitamin D this process may fail. Everybody has some self-reactive
lymphocytes and there are additional mechanisms to deal with them but if central
tolerance is not working well a person can generate a steady stream of strongly
self-reactive lymphocytes.
Every lymphocyte receptor or antibody can either not bind to a substance (antigen)
or can bind with various degrees of strength. An antibody that binds strongly to
an antigen fits like a lock and key or hand and glove. If it binds less strongly,
the fit is only so-so. Antibodies can bind to many places on the gliadin molecule
(part of the gluten molecule). Virtually all of these would show up on gliadin
(gluten) antibody blood test. Maybe 10% of many populations are positive for this.
Now for the MISCONCEPTION. Many people have assumed the gliadin antibody test is
useless because of the above percent and thus gluten Ataxia doesn't exist. Two
gliadin antibodies are not the same unless they are clones. For gluten Ataxia the
only gliadin antibodies of interest are those that also strongly bind (cross react)
to neuro self-antigens. Dr. Alaedini's research shows this to happen on the neuro
protein synapsin. There might be others but his research checked a standard array
of potential neuro self-antigens that are on the outside of cells.
The thoughts about the blood brain barrier are interesting. Keep in mind though, it
doesn't matter if there are gliadin antibodies in the brain unless they are strongly
reacting with brain self-antigens. Thus the simpler explanation for two people
that have high levels of gliadin antibodies but only one has Ataxia is the person
without Ataxia does not have gliadin antibodies that are cross reactive to brain
self-antigens (such as synapsin). Antibodies are not quite as true/false as I used
to think. They can bind in many places and many people's lymphocytes kill themselves
if they are strongly self-reactive. There are also some other mechanisms that may
allow one person with strongly self-reactive gliadin antibodies that may not show
symptoms of Ataxia. There are regulatory lymphocytes (T-reg) that can reduce the
antibody response. It's like two people with an SCA1 gene (same number of CAG
repeats) who develop Ataxia at widely different ages. I suspect many people have
some cerebellar damage such as environmental toxins such as fumes when they were
younger. This may allow clinical Ataxia symptoms to show earlier from another cause
(SCA1 or Gluten Ataxia, or trauma etc.)
I have seen mention of the blood brain barrier in at least one of the papers and
will let you know if I can find it again. You might look in more detail at
Alaedini's presentation from the 2008 NAF annual meeting.
Very Wordy Bear |
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howdy professors ,
well it seems like we are off on a new tangent...this time its the blood brain barrier , what is known to penetrate this barrier ? don't tell me the bovine mad moo cow thing , or aids is said to be another penetrator ( im full of puns today )
microglia has now entered the lexicon , as due acknowledgement has been accorded britannica , wikipedia ect , sundry lecturers / authors known only by their last names , no charge of plagiarism will stick
i shall leave you unmolested ( for now  ) but i do think much disambiguation will be required on the part of your esteemed selves so the more dumberer pooples like me can follow
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Dr. Teddybear,
Nice try professor. You've slipped in the past showing you are not as dumberer as
u wan usun to thimker.
Bear |
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Bear, Yes, Mosby's Is Dated. That's the point. The Fourth Edition Was Published in the Mid-90s . I Was Engaging in a Little Self-Flagellation Because in another one of your threads under news I clearly showed that I did not know what microglia were, or at least forgot I knew.
Mosby's is not a dictionary the docs would use anyway. It is primarily a dictionary for nursing school. If nursing dictionaries listed it in the 90s, docs probably knew about them in the 70s or 80s, at least. I guess to make sure you would have to get an anatomy book used in medical school in the 70s and 80s.
(make that bet post 1970 )
We crack our sliding glass door and the cat can go through the opening but almost no other critter can. (She amazes me because she can actually run through the opening which is just barely wide enough for her to fit. If most people started to run through doorways that they barely fit through, there would probably be a lot of concussions from people running into the wall.) The blood brain barrier is not so much different from our sliding glass door. When it is barely cracked, which is the state that a healthy blood brain barrier is usually in, almost nothing gets through it. (I note your question TB, and it is a good one. My answer is I don't know except for stuff like oxygen and glucose get through. Wikipeia claims that most antibodies CANNOT pass through the BBB.
My question, Bear, is can gliadin antibodies squeeze through the blood brain barrier of a healthy person. (It seems ironic that the antibody tested for in the correct test is actually bigger than the anti-body tested for in the other test.) If the antibody can't squeeze through the barrier, it can't cross react with neurons or what have you.
Just like we can slide our glass door open wider to let more things through, the blood brain barrier can open wider too. If it does, it is usually a sign that something is wrong. I imagine pathogens have various strategies to get the blood brain barrier to "slide the door open some more" or it could just be a genetic flaw or it could be due to something else. So maybe these anti-bodies squeeze through an unhealthy brain blood barrier. That would explain a lot.
ATILLA
Mrs. ATILLA still loves me |
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the least said about self flagulation the better.....this being a family forum n all
cats use their whiskas to judge width in particular
i zink ve should conductum ze experamenta wiz you cat , ve vill call it puddy vor our purposeeez
step 1....cutz ze whiskas one inch of puddy
step 2... close ze zliding door one inch
step 3... make puddy run thruz ze gap ( at gun points eff nezzecary )
ve vill maybees finds out eff ze old zaying " hard as a cats head is true "
a far as the bbb is concerned wiki is correct in saying most things cannot pass the bbb...a few things can ....bovin spongyform encephalophathy( mad cow disease ) caused by infected meat mainly in the uk where beef cattle were fed a mixture of ground up dry themselves as in cannibal eating...in humans BSE is called cruetzfeld-jakob disease (a nerological condition ) and CJD variants...up to a 4 year incubation period complicates where and when a person consumed infected beef
prior health has no bearing with CJD ...those unlucky enough to eat the wrong burger or are one of the unexplained sporadic cases have only about 6 months.....CJD is fatal in all cases
when donating blood here the question is asked if you were in the uk between certain years when BSE was more active
AIDS is said to pass the BBB , this makes it hard to target as a virus in that how do you get any anti virus past the BBB.......this is all i know or think i know of the BBB
vee expeccct za full reportz on ze puddy experamentzz
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Bear
I do not doubt the accuracy of your position that it is the old aminated test is the correct one.
Can you provide any links or research papers that reinforce this.
I have done internet searches to find more information about this. I am unable to find anything that reinforces this. Or Dr Aleadani's research paper on the subject?
In order to get my doctor to order from a specific lab for a specific kind of test, I am sure that I will need something more substantial than your post to the discussion board.
Gluten tests are generally conducted at the in-house lab at the doctor that I go to.
I have 2 doctors. One is doing a fellowship under the other.
I am able to correspond by email with my doctor(the fellow) and she was non responsive to my question whether the test was aminated or deaminated. She only responded that I was not Gluten sensitive.
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Hi Oldtimer,
I think it is unlikely you will find a research paper. We are in the process of
submitting a letter to a journal to document this and I don't know if it will be
accepted. If it is accepted there can be a long lag time.
We discovered it by accident. Mrs. Bear feels like a pincushion because to track
the progress of her Ataxia, she has had a periodic set of gliadin antibody tests
over the last 5 years. Over time her gliadin antibody values have hopped around
with an average downward trend. All of a sudden she got several tests in a row with
the same value of less than 1 (could be zero). After the fourth test I got
suspicious, investigated and found they had substituted in the deamidated gliadin Ab
test without telling us. The next time the doctor specified the original test by
specifying the exact Quest test number. Sure enough the values from the original
test were well above zero.
The problem is the new test is better for testing for Celiac Disease and some of
those people also have Gluten Ataxia. However, you can have Gluten Ataxia and not
Celiac Disease (like Mrs. Bear). You could tell the doc you want the original
test. If you get a very low value on the original test, you don't have Gluten
Ataxia, if you get a very low value on the newer deamidated test, you don't really
know whether you might have Gluten Ataxia or not. If you need more ammo, you
could email me at ataxiabear
AT
yahoo.com
(you have to put the pieces together from the above three lines for the email)
Let me know with a post if you do because I don't check the account very often.
Bear |
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Bear, can you share who is we?
ATILLA
Mrs. ATILLA still loves me |
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Bear
Can you say what journal it is and approximitley when it will be published? |
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Bear
Can you say what journal it is and approximitley when it will be published? |
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Hi Oldtimer,
I slipped and said "We are in the PROCESS of submitting a letter". That means it
has not been sent yet - lots of editing, picky formatting and citing references
before it is ready. Then it has to be accepted (or not!). If we get past that
hurdle, it will probably take months. I will post when/where it will appear if we
can get it accepted.
Bear
P.S.It is not a paper, only a letter detailing the deamidated issue. |
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Bear, is there a theory why one test is better?
ATILLA
Mrs. ATILLA still loves me |
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ATILLA,
I think it is either because the deamidated gliadin IgG antibody is concentrated near
the intestines and/or they do not have the right shape to fit the same
neuro-proteins as the gliadin antibodies. I'll have to check on that one of these
days.
Note, which test is better is not quite the right question. The deamidated gliadin
antibody is better for problems with the intestines (celiac disease). The original
gliadin antibody is probably better for neurological problems.
The issue only came about because Mrs. Bear had four deamidated gliadin IgG tests
in a row all with the same value of less than 1 (probably zero). All the same
value and close to or equal to zero is a big red flag something is wrong. The
original tests before and after had changing values and were always well above
zero. I don't think there has been any formal testing of the deamidated test for
detecting Gluten Ataxia.
Bear |
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| Bump for Micaryan, Romney. Bear |
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| HEY! Duh Forgot to look at this before travels but didn't expect kids to be tested....oh well. Kids had IgA and Ttg testing done - no clue on where it's going or who's test is being run. |
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Hi Kelly,
TTg, they are testing for Celiac Disease. If you get the test sheet from the lab you
can probably figure out what was run for the IgA.
Super mom, just in case you forgot, you do have a "few" other things to remember
and keep track of. Fortunately your kids are very passive and quiet all the time.
Bear |
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