Lab test results.. help!

[Guest guest]

Glad to help. Let us know if you need help deciphering your results.

Me Me!! :::waving wildly::: I just picked mine up from the dr. but it's like looking at Chinese.

Although, I don't even know where to start or what you need..

Tissue Transglutaminase Antibody

TTG IGA AB 0.6 F AU

TTG IGA AB..... 08/04/06 1437

Reference Interval: Tissue Transglutaminase Antibody, IgA

Age Negative Positive

0-1 yr Less than 5.0 AU 5.0 AU or greater

2 yrs and older Less than 7.0 AU 7.0 AU or greater

Miscellanous testing

IGA 255 F mg/dl 68-378

IGA.....................................08-04-06 1437 Tissue transglutaminase antibody, IgA (00-97709) to follow.

(That number 255 is circled on my lab results and it is written in pen "good" next to it. also the 0.6 up by the TTG IGA AB was circled. Apparently as long as that .6 number was less than 7.0 I'm good and the 255 number is between 68 and 378 I'm good. That's what I get from it anyway.)

Any thoughts? Does it matter that all I ate that day was a half a bagel about 2 hrs before? I doubt it but thought I should ask if eating affects the results.

KATIE B.Happy Summer

[Guest guest]

I am not a Dr, but it looks like you are

negative for the anti tissue transglutaminase IgA,. The IgA result of 255

refers to a total serum IgA, and lets you know that you are NOT IgA deficent –

which is good. It should not matter what or how much you ate the day of

the test.

Suzie

From: SillyYaks [mailto:SillyYaks ] On Behalf Of sendn9112u@...

Sent: Wednesday, August 16, 2006

5:25 PM

To: SillyYaks

Subject: Lab test

results.. help!

Glad to help. Let us know if you need

help deciphering your results.

Me Me!! :::waving wildly::: I just

picked mine up from the dr. but it's like looking at Chinese.

Although, I don't even know where to

start or what you need..

Tissue Transglutaminase Antibody

TTG IGA

AB

0.6

F

AU

TTG IGA AB..... 08/04/06 1437

Reference Interval: Tissue Transglutaminase Antibody, IgA

Age

Negative

Positive

0-1

yr Less

than 5.0 AU

5.0 AU or greater

2 yrs and

older

Less than 7.0 AU

7.0 AU or greater

Miscellanous testing

IGA 255

F

mg/dl 68-378

IGA.....................................08-04-06

1437 Tissue transglutaminase antibody, IgA (00-97709) to follow.

(That number 255 is circled on my lab

results and it is written in pen " good " next to it. also the 0.6 up

by the TTG IGA AB was circled. Apparently as long as that .6 number was less

than 7.0 I'm good and the 255 number is between 68 and 378 I'm good. That's

what I get from it anyway.)

Any thoughts? Does it matter that all I

ate that day was a half a bagel about 2 hrs before? I doubt it but thought I

should ask if eating affects the results.

KATIE B.

Happy Summer

[Guest guest]

So because I did have the IgA test, then it's for sure I don't have it? Or can I still? I'm so confused. I can be a carrier of the gene but not test positive? Or because I did test positive I don't need the genetic testing? I know, I'm new to this, bear with me.

I am not a Dr, but it looks like you are negative for the anti tissue transglutaminase IgA,. The IgA result of 255 refers to a total serum IgA, and lets you know that you are NOT IgA deficent – which is good. It should not matter what or how much you ate the day of the test.

Suzie

KATIE B.Happy Summer

[Guest guest]

You could have gluten intolerance and yet not have it show

on the blood tests nor on endoscopy.

If you've

- taken all the blood tests and they are negative, and

- if you've had an endoscopy and it was negative,

and yet you

- carry the gene, and

- are not feeling well

then I would suggest going Gluten Free to see if it helps.

It can't hurt, especially if you've already taken the blood

tests and the endoscopy.

The tests are not perfect. The celiac can still be there even

if you aren't " sick enough " for the tests to show it.

If one is CLEARLY undeniably celiac (ie, total intestinal meltdown),

then the tests will surely show it.

But there are many of us who are " sub-clinical " . We are sick and

miserable and yet " pass " the tests.

The REAL test is whether avoiding all gluten helps you.

If it does, you have your answer.

If it doesn't, and you are sure you have ALL traces of gluten

out of your diet, then your doctor needs to keep looking for

other causes of misery.

Here's to hoping that GF eating will make you feel like a

Superheroine in no time.

I felt better within days. Days, I tell you. It was a miracle.

Esther in RI

ps, the total IGA test showed you are not IGA deficient. If one

is IGA deficient, then one can " artificially pass " the other

IGA-based antibody tests. But since you are NOT IGA-deficient,

that means they can trust the numbers they got for the other

IGA antibodies. Yes, it's VERY confusing. I didn't learn about

this stuff until I started going down the road of having my

kids tested.

>

>

>

> So because I did have the IgA test, then it's for sure I don't have

it? Or

> can I still? I'm so confused. I can be a carrier of the gene but not

test

> positive? Or because I did test positive I don't need the genetic

testing? I

> know, I'm new to this, bear with me.

>

> I am not a Dr, but it looks like you are negative for the anti tissue

> transglutaminase IgA,. The IgA result of 255 refers to a total

serum IgA, and lets

> you know that you are NOT IgA deficent †" which is good. It

should not

> matter what or how much you ate the day of the test.

> Suzie

>

>

>

>

>

>

>

> KATIE B.

> Happy Summer

>

[Guest guest]

, my daughter and both had negative blood tests. The blood tests can come

back negative in over 50% of the cases. My daughter is the only one of us that

had the biopsy and that showed inflamed villi.

Yes, you can still have it. I think the only sure way to know that is the diet.

My daughter health did a complete turnaround after going gluten free.

Zanna

http://groups.yahoo.com/group/Art_on_A_Budget/

My daily rantings!

www.zannasstory.blogspot.com

My picture trail:

www.picturetrail.com/xanadoodles

[Guest guest]

Thank you for taking the time to explain all that! I was glad I had my coffee for the morning before reading it, and I'll have to read it again but thank you. I really wish you were my brother, or cousin or neighbor so you could look at all the test results my dr's run and tell me what the heck they mean since I woke up today with my muscle soreness back again and I feel devastated. Thanks for taking the time though!

People who carry the DQ2.5 haplotype have a higher tendency tobe IgA less. IgA less means testing IgA-tTG is non-informativeand IgG-tTG. A person can have protoGSE and have low tTG, thetTG is concentrated in the deposits in the small bowel. In terms of your test results if the 0.6 is a correctassay results, it is very unlikely you have elevated tTGanywhere. The genetic predispositions for GSE areDQ2.5 (about 90%) of CDDQ8 (about 20%) of CDDQ2.2/DQ7.55 (less than 5%) of CD~35% of the normal population has these genetic susceptibilitiesTherefore having one of these only increase risk by 150%Or to put otherwise 1:133 individuals have GSE, but ifyou have any of these three types your risk is ~1:46, if weconsider protoGSE conditions which are currently undiagnosablein the western hemisphere the risk is about 1:40.If you have not been typed for and have any of thesethree you don't know what your unweighed predisposition is. If you have been typed for these and you have:1. Family members with GSE2. Autoimmune disease, anemia, GI problems, Then your predisposition increases. If you have a family member with CD but you are DQ"-"you risk is low, as the general population. If you have a family member with CD and you are DQ"+"and no symptome your risk is 1 in 8If you are in a family in which several members andseveral generations show some CD and you are DQ"+"risk is markedly increased. Could be as high as 1:3In other families the risk is as the general population.

KATIE B.Happy Summer

[Guest guest]

>

>

>

> So because I did have the IgA test, then it's for sure I don't have

it? Or

> can I still? I'm so confused. I can be a carrier of the gene but

not test

> positive? Or because I did test positive I don't need the genetic

testing? I

> know, I'm new to this, bear with me.

People who carry the DQ2.5 haplotype have a higher tendency to

be IgA less. IgA less means testing IgA-tTG is non-informative

and IgG-tTG. A person can have protoGSE and have low tTG, the

tTG is concentrated in the deposits in the small bowel.

In terms of your test results if the 0.6 is a correct

assay results, it is very unlikely you have elevated tTG

anywhere.

The genetic predispositions for GSE are

DQ2.5 (about 90%) of CD

DQ8 (about 20%) of CD

DQ2.2/DQ7.55 (less than 5%) of CD

~35% of the normal population has these genetic susceptibilities

Therefore having one of these only increase risk by 150%

Or to put otherwise 1:133 individuals have GSE, but if

you have any of these three types your risk is ~1:46, if we

consider protoGSE conditions which are currently undiagnosable

in the western hemisphere the risk is about 1:40.

If you have not been typed for and have any of these

three you don't know what your unweighed predisposition is.

If you have been typed for these and you have:

1. Family members with GSE

2. Autoimmune disease, anemia, GI problems,

Then your predisposition increases.

If you have a family member with CD but you are DQ " - "

you risk is low, as the general population.

If you have a family member with CD and you are DQ " + "

and no symptome your risk is 1 in 8

If you are in a family in which several members and

several generations show some CD and you are DQ " + "

risk is markedly increased. Could be as high as 1:3

In other families the risk is as the general population.

[Guest guest]

Philip, you are always full of amazing information.

I always know to fetch another cup of coffee when I see your

name on an article, though. I need EVERY NEURON fully charged up

to appreciate what you're trying to tell me. HA HA! Esther

>

> ...

> The genetic predispositions for GSE are

> DQ2.5 (about 90%) of CD

> DQ8 (about 20%) of CD

> DQ2.2/DQ7.55 (less than 5%) of CD

> ~35% of the normal population has these genetic susceptibilities

> Therefore having one of these only increase risk by 150%

> Or to put otherwise 1:133 individuals have GSE, but if

> you have any of these three types your risk is ~1:46, if we

> consider protoGSE conditions which are currently undiagnosable

> in the western hemisphere the risk is about 1:40.

>

> ...

[Guest guest]

>

> , my daughter and both had negative blood tests. The blood

tests can come back negative in over 50% of the cases. My daughter

is the only one of us that had the biopsy and that showed inflamed

villi.

>

> Yes, you can still have it. I think the only sure way to know that

is the diet. My daughter health did a complete turnaround after

going gluten free.

In the 1950s before they the villus biopsy (1957) the way they

diagnosed the disease was to take the person off of gluten (triticeae)

and observe the person (generally a child since intolerance in adults

was not generally recongnized until later)

then in 2 or three weeks do a gluten challenge, observe.

Some of the reports show them turning on and off CD like a

switch. Typical scenario was:

On gluten challenge

discomfort

diarrhea

steatorrhoea (fat in the feces)

abdominal distention and flatus

emaciation

On gluten ceasation

discomfort disappeared (ussually in 3 days)

diarrhea stopped, flatus stopped

abdominal normal, apetite returned (week or so)

steatorrhoea subsided

children rapidly regained loss muscle mass.

You do this 2 or 3 times and parent, children got the picture.

Cured!

There was one adult case, I think it was 1954 or so, female, long

history of clinical problems, anemia, emaciation, claims to had

symptoms since 1940 or so, in 1953 or so she entered the clinic

at 85 lbs, was basically moribund and near death. She was placed

on a gluten free diet, within 3 weeks she left the hospital as

healthy as she claimed 'in 15 years' within 6 months was up to 142

lbs.

I don't don't think any of the physicians after that seriously

questioned that adult idiopathic steatorhoea was different to coeliac

disease other than there were two onset distributions that barely

overlapped. Childhood onset was 7mos to 2 years, mean about 10 mos.

Adult onset was 18 to 50 years with a mean about 28. Before that

physicians were trying to find any excuse why the individual had

gone to the tropics as to get rid of this inexplicable catagory.

The other big difference is that the children responded much more

rapidly to gluten cessation relative to adults. Therefore the gluten

challenge is more problematic relative to adults. You may not

get a clear answer in biopsy and you may be doing significant long

term damage.

Whats happening now is interesting. What they are seeing is why

there are clinical 'violations' of the standards, particularly

tTG.

We all know that the gold standard is biopsy, but with patchy villous

atropy unless a serios gluten challenge is done, biopsy may not

detect an abnormality.

Chronic late onset cases present a clinical challenge, because now it

is believed that anti-Gliadin goes up, then comes down, anti-tTG goes

up then goes down and tTG becomes non systemic, a reason why

antibodies to EMA are often present when anti-tTG is not, the

antibodies are locked into a very specific local response. Therefore

the clinical diagnosis in some severe late onset cases (severe

meaning constant damamge and stimulation has occurred) may go

undiagnoses at several levels.

So now the molecular biology of tTG has suddenly become

interesting, and I suspect the cellular immunochemisty will soon

follow.

Common sense is sometimes good. When asked I have said exactly

this, the difference between GSE and protoGSE exists mainly in the

mind of the clinician, the clinician being generally unawars of

the protoGSE condition. In that instance if you are challenged and

you are just short of needing to go to the hospital or emergency rooms

with some symptomology (acute pain, nausea, increased smelly flatus,

cerebral ataxia, anemia) and you do not get a positive diagnosis.

I would listen to my body, 3 of 24 patients in the finnish study had

a secondary autoimmune condition, 3 of 24 had anemia, family members

with CD, and 17 of 24 had Gi symptoms, of these that were DQ " + " and

showed signs of elevated IEL. 10 of 11 that had negative tTG and

biopsies showed up with anti-tTG IgA deposits in the epithelia.

Somehow the signal of these very cryptic events in the epithelia is

making the individual feel sick and causing other secondary diseases.

As a result common sense would tell an individual who has a bad

reaction to gluten, but unlikely to enter a finnish study group, that

the best choice is to go GF.

But even in individuals who have tTG antibodies deposits a tTG IgA

some systemic, subclinical anti-tTG exists on their scale 7 is

considered clinical so at 1/10th the clinical level, if the test

was good, then I would say the risk of CD is low or outside the

confidence range for subclinical CD+clinical CD. A point needs to

be made about Finegold's testing. If it is true that tTG Abs are

restricted to the epithelia and that gliadin causes the sloughing of

villi and partial digestion of tTG [_IF_] disease specific antibodies

could, should be higher in the feces relative to normal individuals.

And in particular if the condition causes maladsorption that proceeds

into the distal small intestine then the likelihood that it would be

increased in feces and potentially much higher than blood is not only

plausible but probable. A decade ago we developed 2 monoclonal

antibodies against human hemoglobin we used the antibodies to screen

hemoglobin in the feces based on several GI conditions. The binding

of the antibodies clearly distinguished lower GI bleeding (complete

reactivity) with upper GI bleeding (reduced or none-stomach). Thus a

maladsorption disease predicts active antibodies of intestinal origin

in the feces.

[Guest guest]

My first problem was severe respiratory allergies, then the onset of an itchy, blistery rash about 1953. The dermatologist/allergist treated my for 3 years and his diagnosis was hypochondria, anxiety. My family physician decided the best thing was to take me to the ocean and allow me to swim several times a day. Which my parents did and the whole rash (which was extensive over most of my extremities) began to recede and flake off like cornflakes. But after several years of gluten, when I was in college, it began to reappear. Actually, the dermatologist was on the right track when he took me off wheat for 3 weeks, but that's not enough for a person with DH to heal. And since I was so painfully thin he decided to allow me to go back on wheat. It only took them 53 years to figure out what was wrong with me and that was because I figured it out and asked the doctor for the testing. By that time my intestinal tract was so involved

that my whole immune system has been compromised. I certainly hope that geneticists can figure this whole scenario out and help future generations to take care of their systems. A healthy immune system was what I and many of us are born with, but the ingestion of wheat and related products can cause us to end up with a totally compromised immune system. Shirley in San DiegoPhilip Deitiker wrote: >> , my daughter and both had negative blood tests. The blood tests can come back negative in over 50% of the cases. My daughter is the only one of us that had the biopsy and that showed inflamed villi.> > Yes, you can still have it. I think the only sure way to know that is the diet. My daughter health did a complete turnaround after going gluten free.In the 1950s before they the villus biopsy (1957) the way theydiagnosed the disease was to take the person off of gluten (triticeae)and observe the person (generally a child since intolerance in adultswas not generally recongnized until later)then in 2 or three weeks do a gluten challenge, observe.Some of the reports show them turning on and off CD like aswitch. Typical scenario was:On gluten challenge discomfortdiarrheasteatorrhoea (fat in the feces)abdominal distention and

flatusemaciation On gluten ceasationdiscomfort disappeared (ussually in 3 days)diarrhea stopped, flatus stoppedabdominal normal, apetite returned (week or so)steatorrhoea subsidedchildren rapidly regained loss muscle mass. You do this 2 or 3 times and parent, children got the picture. Cured!There was one adult case, I think it was 1954 or so, female, longhistory of clinical problems, anemia, emaciation, claims to had symptoms since 1940 or so, in 1953 or so she entered the clinicat 85 lbs, was basically moribund and near death. She was placedon a gluten free diet, within 3 weeks she left the hospital ashealthy as she claimed 'in 15 years' within 6 months was up to 142lbs. I don't don't think any of the physicians after that seriously questioned that adult idiopathic steatorhoea was different to coeliac disease other than there were two onset distributions that barely overlapped.

Childhood onset was 7mos to 2 years, mean about 10 mos. Adult onset was 18 to 50 years with a mean about 28. Before that physicians were trying to find any excuse why the individual hadgone to the tropics as to get rid of this inexplicable catagory. The other big difference is that the children responded much morerapidly to gluten cessation relative to adults. Therefore the glutenchallenge is more problematic relative to adults. You may notget a clear answer in biopsy and you may be doing significant longterm damage. Whats happening now is interesting. What they are seeing is whythere are clinical 'violations' of the standards, particularlytTG. We all know that the gold standard is biopsy, but with patchy villousatropy unless a serios gluten challenge is done, biopsy may not detect an abnormality. Chronic late onset cases present a clinical challenge, because now it is believed that

anti-Gliadin goes up, then comes down, anti-tTG goes up then goes down and tTG becomes non systemic, a reason why antibodies to EMA are often present when anti-tTG is not, the antibodies are locked into a very specific local response. Thereforethe clinical diagnosis in some severe late onset cases (severe meaning constant damamge and stimulation has occurred) may go undiagnoses at several levels. So now the molecular biology of tTG has suddenly become interesting, and I suspect the cellular immunochemisty will soonfollow. Common sense is sometimes good. When asked I have said exactlythis, the difference between GSE and protoGSE exists mainly in the mind of the clinician, the clinician being generally unawars of the protoGSE condition. In that instance if you are challenged andyou are just short of needing to go to the hospital or emergency roomswith some symptomology (acute pain, nausea, increased smelly

flatus, cerebral ataxia, anemia) and you do not get a positive diagnosis. I would listen to my body, 3 of 24 patients in the finnish study had a secondary autoimmune condition, 3 of 24 had anemia, family members with CD, and 17 of 24 had Gi symptoms, of these that were DQ"+" and showed signs of elevated IEL. 10 of 11 that had negative tTG and biopsies showed up with anti-tTG IgA deposits in the epithelia. Somehow the signal of these very cryptic events in the epithelia is making the individual feel sick and causing other secondary diseases. As a result common sense would tell an individual who has a badreaction to gluten, but unlikely to enter a finnish study group, that the best choice is to go GF. But even in individuals who have tTG antibodies deposits a tTG IgA some systemic, subclinical anti-tTG exists on their scale 7 is considered clinical so at 1/10th the clinical level, if the testwas good, then I

would say the risk of CD is low or outside the confidence range for subclinical CD+clinical CD. A point needs tobe made about Finegold's testing. If it is true that tTG Abs are restricted to the epithelia and that gliadin causes the sloughing of villi and partial digestion of tTG [_IF_] disease specific antibodies could, should be higher in the feces relative to normal individuals. And in particular if the condition causes maladsorption that proceeds into the distal small intestine then the likelihood that it would be increased in feces and potentially much higher than blood is not only plausible but probable. A decade ago we developed 2 monoclonal antibodies against human hemoglobin we used the antibodies to screen hemoglobin in the feces based on several GI conditions. The binding of the antibodies clearly distinguished lower GI bleeding (complete reactivity) with upper GI bleeding (reduced or none-stomach). Thus a

maladsorption disease predicts active antibodies of intestinal origin in the feces.