Aa
Gluten Free and Celiac
I have reposted this as it seems that some mebers here feel that if they are Gluten Intolerant that they have CELIAC Disease which isnt always the case.
Some give up Gluten on the 'pretence' that this will CURE their Hashimoto's antibodies which is totally UNTRUE.
Celiac and Gluten Intolerance are two DIFFERENT conditions.
This is to show all those that Hashi's is NOT CURABLE by going Gluten Free contray to some members postings here.
With CELIAC..... IGg antibodies can be suppressed through NOT eating Wheat and/or Gluten.
This is NOT Hashi antibodies.
Anti-gliadin, anti-endomysium, and anti-transglutaminase antibodys are the main antibodys in Celiac and these are what are tested for in Celiac Disease.
There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus.
The minimum is 2 slices of bread per day for 6 weeks to get an accurate test. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc.
We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal serum in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies.
Just because you are Gluten Intolerant this does NOT mean you have Celiac .
As I said..this is one misconception I would like to clear up after recent postings of other members.
Some give up Gluten on the 'pretence' that this will CURE their Hashimoto's antibodies which is totally UNTRUE.
Celiac and Gluten Intolerance are two DIFFERENT conditions.
This is to show all those that Hashi's is NOT CURABLE by going Gluten Free contray to some members postings here.
With CELIAC..... IGg antibodies can be suppressed through NOT eating Wheat and/or Gluten.
This is NOT Hashi antibodies.
Anti-gliadin, anti-endomysium, and anti-transglutaminase antibodys are the main antibodys in Celiac and these are what are tested for in Celiac Disease.
There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus.
The minimum is 2 slices of bread per day for 6 weeks to get an accurate test. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc.
We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal serum in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies.
Just because you are Gluten Intolerant this does NOT mean you have Celiac .
As I said..this is one misconception I would like to clear up after recent postings of other members.
So if anyone wants to know if they HAVE any other AUTOIMMUNE DISEASES......ask for a C1-9 panel (complementary panel).
I dont know the cost as Australia covers these tests in Major Hospitals and Specialists.
I dont know the cost as Australia covers these tests in Major Hospitals and Specialists.
I have slept, ate and breathed G/F for the past few days lol.
Thanks for all this info. especially the clarification between antibodies and antigens. Makes better sense now.
Lots of info, would be good in the health pages even though its not thyroid. You know this will come up again!
This has nothing to do with TH1 and TH2 .
Antibodys are autoimmune...Antigens arent.
Celiac is ANTIBODYS
Gluten Intolerance is ANTIGENS
Antigens are allergys and can be fixed by removal of food/toxins causing them.
Antibodys cannot be fixed.
See the difference?
This is where people are getting confused ...antigens are NOT antibodys lol
Antibodys are autoimmune...Antigens arent.
Celiac is ANTIBODYS
Gluten Intolerance is ANTIGENS
Antigens are allergys and can be fixed by removal of food/toxins causing them.
Antibodys cannot be fixed.
See the difference?
This is where people are getting confused ...antigens are NOT antibodys lol
Which IG levels came back as high?
And......this is what I was told when I was tested for Celiac and any other Autoimmune Diseases. This information was given to me by a Molecular Scientist and a Top Allergist in Melbourne, Australia and was given to me in March 2010 so is cureently resent research.
I was given a Complementry Full Blood Panel which showed up Graves Disease and no other Autoimmune Disease. The main reason for this panel of labs was to rule out Celiac.
This DOES NOT rule out NCGI (Non Celiac Gluten Intolerant. Rather it determines the DIFFERENCE between ANTIGENS and ANTIBODIES,
That being the difference in Autoimmune Celiac and Non Celiac Gluten Intolerance.
I hope it makes sense...as I had to go over it a few times to fully understand it.
.
The complement system is a set of circulating blood proteins that work together to promote immune and inflammatory responses. Their principal role is to destroy foreign substances like bacteria and viruses. The nine primary complement components are those designated as C1 through C9. They are assisted and regulated by several subcomponents and inhibitors.
The complement system is part of the bodys innate immune system. Unlike the acquired immune system, which produces antibodies that target and protect against specific threats, the innate immune system is non-specific and can quickly respond to foreign substances (Gluten). It does not require advance exposure to an invading microorganism or substance and does not maintain a memory of previous encounters. As part of the innate immune system, the complement system has evolved to recognise antigen-antibody complexes (immune complexes) as well as certain structures and polysaccharides (complex carbohydrates) found on the outside membranes of microorganisms and other foreign cells.
Complement activation may be initiated in several different ways. These are termed classical, alternative or lectin pathways. However, the final product from all activation pathways is the same the formation of the Membrane Attack Complex (MAC)
Complement activation causes several things to happen:
• The MAC binds to the surface of each microorganism or abnormal cell that has been targeted for destruction. It creates a lesion (hole) in the membrane wall, and causes lysis, which is destruction of the cell by letting the contents out like piercing a water-filled balloon.
• It increases the permeability of blood vessels, allowing white blood cells (WBCs) to move out of the bloodstream and into the tissues.
• It attracts WBCs to the site of the infection.
• It stimulates phagocytosis, a process in which microorganisms are engulfed by macrophages and neutrophils and killed.
• It increases the solubility of the immune complexes and helps to clear them out of the serum.
Complement proteins both promote and regulate these activities. Inherited or acquired deficiencies or abnormalities in one or more of the complement components may adversely affect the integrity and function of the immune system. Deficiencies may also arise because of decreased production or increased use of one or more complement proteins.
These tests measure the quantity or the function (activity) of complement proteins in the blood. Complement components may be measured individually and together to determine whether the system is functioning normally. C3 and C4 are the most frequently measured complement proteins. Total complement activity (CH50, or CH100) can be measured if the doctor suspects a deficiency that is not measured by C3 or C4. CH50 measures the function of the complete classical complement pathway, C1 C9. If this measurement is outside the normal range, then each of the 9 different complement levels can be measured individually to look for hereditary or acquired deficiencies.
I was given a Complementry Full Blood Panel which showed up Graves Disease and no other Autoimmune Disease. The main reason for this panel of labs was to rule out Celiac.
This DOES NOT rule out NCGI (Non Celiac Gluten Intolerant. Rather it determines the DIFFERENCE between ANTIGENS and ANTIBODIES,
That being the difference in Autoimmune Celiac and Non Celiac Gluten Intolerance.
I hope it makes sense...as I had to go over it a few times to fully understand it.
.
The complement system is a set of circulating blood proteins that work together to promote immune and inflammatory responses. Their principal role is to destroy foreign substances like bacteria and viruses. The nine primary complement components are those designated as C1 through C9. They are assisted and regulated by several subcomponents and inhibitors.
The complement system is part of the bodys innate immune system. Unlike the acquired immune system, which produces antibodies that target and protect against specific threats, the innate immune system is non-specific and can quickly respond to foreign substances (Gluten). It does not require advance exposure to an invading microorganism or substance and does not maintain a memory of previous encounters. As part of the innate immune system, the complement system has evolved to recognise antigen-antibody complexes (immune complexes) as well as certain structures and polysaccharides (complex carbohydrates) found on the outside membranes of microorganisms and other foreign cells.
Complement activation may be initiated in several different ways. These are termed classical, alternative or lectin pathways. However, the final product from all activation pathways is the same the formation of the Membrane Attack Complex (MAC)
Complement activation causes several things to happen:
• The MAC binds to the surface of each microorganism or abnormal cell that has been targeted for destruction. It creates a lesion (hole) in the membrane wall, and causes lysis, which is destruction of the cell by letting the contents out like piercing a water-filled balloon.
• It increases the permeability of blood vessels, allowing white blood cells (WBCs) to move out of the bloodstream and into the tissues.
• It attracts WBCs to the site of the infection.
• It stimulates phagocytosis, a process in which microorganisms are engulfed by macrophages and neutrophils and killed.
• It increases the solubility of the immune complexes and helps to clear them out of the serum.
Complement proteins both promote and regulate these activities. Inherited or acquired deficiencies or abnormalities in one or more of the complement components may adversely affect the integrity and function of the immune system. Deficiencies may also arise because of decreased production or increased use of one or more complement proteins.
These tests measure the quantity or the function (activity) of complement proteins in the blood. Complement components may be measured individually and together to determine whether the system is functioning normally. C3 and C4 are the most frequently measured complement proteins. Total complement activity (CH50, or CH100) can be measured if the doctor suspects a deficiency that is not measured by C3 or C4. CH50 measures the function of the complete classical complement pathway, C1 C9. If this measurement is outside the normal range, then each of the 9 different complement levels can be measured individually to look for hereditary or acquired deficiencies.
Part Two
Endomysial Antibodies:
IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge.
The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies.
Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out.
In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with:
* An initial positive gut biopsy;
* 6 months on a gluten free diet;
* A second, negative gut biopsy;
* A gluten challenge for 6 months and;
* A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure.
Endomysial Antibodies:
IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge.
The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies.
Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out.
In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with:
* An initial positive gut biopsy;
* 6 months on a gluten free diet;
* A second, negative gut biopsy;
* A gluten challenge for 6 months and;
* A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure.
Here is what I found. I might add that I am no expert on Celiac and Gluten Intolerant even though I am in the medical field.
Anti-Gliadin Antibodies:
Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results.
A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower.
My posting is in TWO parts as it exceeds the limit of words.
Anti-Gliadin Antibodies:
Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results.
A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower.
My posting is in TWO parts as it exceeds the limit of words.
COMMUNITY LEADER
I vote for NCGI ----
Like hypothyroid and Hashi hypothyroid.
I try to call just hypothyroid "regular hypothyroid" but maybe non-Hashi hypothyroid is more self explanatory. Regular hypo has no official name other than hypothyroid, and some here did / or do not know the difference was antibodies.
So yes "non-celiac gluten intolerance" is better, but thats more typing (not my skill set)! LOL.
I try to call just hypothyroid "regular hypothyroid" but maybe non-Hashi hypothyroid is more self explanatory. Regular hypo has no official name other than hypothyroid, and some here did / or do not know the difference was antibodies.
So yes "non-celiac gluten intolerance" is better, but thats more typing (not my skill set)! LOL.
Just last week I was reading a study (old), and right at the beginning it stated "...celiac, also called 'gluten intolerance'...". So, the distinction is recent. I've been trying to always say "non-celiac gluten intolerance" (puff!) lately. I think if you don't specify all that, you ARE going to have misinterpretation.
Yes, VERY good point. In one on the other posts a member thoght it was the same, asking about gluten intolerance antibodies and was informed they dont exist. Some are not aware of the difference.
Also there is sometimes great pain in Celiac, the intestine is literally in disintegration mode in really bad cases and can even cause death. Intolerance as all should know, is not like that at all.
I just assumed that the difference between Celiac (with antibodies) and Gluten Intolerance (Sensitivity) was well known. Celiac is a disease. GI is not. So much for assuming! On the other hand I never knew they were used interchangeably at one point in time.
Also there is sometimes great pain in Celiac, the intestine is literally in disintegration mode in really bad cases and can even cause death. Intolerance as all should know, is not like that at all.
I just assumed that the difference between Celiac (with antibodies) and Gluten Intolerance (Sensitivity) was well known. Celiac is a disease. GI is not. So much for assuming! On the other hand I never knew they were used interchangeably at one point in time.
I'd like to add that the distinction between gluten intolerance and celiac is further blurred by the fact that the terms USED to be interchageable. If you read older studies (pre-g/f craze), they often list "gluten intolerance" as an alternative term for celiac. So, yes, Deb, it's very important that our language evolve with the times, and we're very specific about which we're discussing.
"Non-celiac gluten intolerance" is a bit cumbersome. We need another acronym, don't we? Perhaps "NCGI"?
"Non-celiac gluten intolerance" is a bit cumbersome. We need another acronym, don't we? Perhaps "NCGI"?
COMMUNITY LEADER
I think Deb would be the person to answer that since she's got the medical background for that type of thing. I know saliva tests are very worthwhile for some things, but not others. Not sure if this is one of them or not.
Maybe if a saliva test shows high gliadin, you should talk to your doctor about the proper blood work; I think you would also want to be tested for gliadin antibodies, as those would tell if the disease are there.
Maybe if a saliva test shows high gliadin, you should talk to your doctor about the proper blood work; I think you would also want to be tested for gliadin antibodies, as those would tell if the disease are there.
Does it mean anything on labs if the gliadin level comes back high? (24 hour saliva test)
Very true Barb.
People read about gluten intolerance and straight away think they have Celiac....which just isnt the case.And Celiac antibodies are COMPLETELY different from thyroid antibodies.
People read about gluten intolerance and straight away think they have Celiac....which just isnt the case.And Celiac antibodies are COMPLETELY different from thyroid antibodies.
COMMUNITY LEADER
Sorry, I hit the "post" button too soon -- I meant to point out that I had brought this up in another thread yesterday. A problem is that too often gluten intolerance is equated with celiac, when they are actually 2 different things..
I appreciate your pointing out those things.
I appreciate your pointing out those things.
COMMUNITY LEADER
I found a site that breaks "gluten intolerance" down into 3 distinct categories: Celiac Disease, Non-Celiac Gluten Sensitivity and a Wheat Allergy.
As we know, celiac is an autoimmune, in which antibodies are produced; non-celiac gluten sensitivity is a bit more vague because there are no antibodies. Wheat allergy has nothing to the the other two. In both celiac and non celiac sensitivity, symptoms come on over a period of time; if one has a wheat allergy, symptoms come on very swiftly. I used to work with a guy who had wheat allergy, but he did not have celiac......
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