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Dh Flare Again.
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31 posts in this topic

I am not a fellow DH sufferer, but I can tell you from what I have read on here from those who are, DH takes longer to resolve than practically everything else. Just when you think you have it licked, it pops up again and says, Here I am!!! Sorry to have to be the bearer of bad tidings but if you talk to Adalaide or pricklypear, or squirmingitch, they will tell you. I feel for you, I really do, but not having been in your shoes I do not know the full extent of the hell that is DH. Stay the course, beware the iodine, and this, too, shall pass. :)

Not exactly great news but, thank you for your caring. :)

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Hi Itch Be Gone,

Oh hon, sorry to say that you'll be in for the long haul. It most surely sounds like dh. You see, what happens is that the antibodies get deposited under our skin & it takes a LONG time for them to get out of our skin. Professional sources say 2 years --- some say up to (gasp) 10 years. Until that time our rash can flare even though we are strict gluten-free & low iodine. And because of this, it is imperative for us to make sure we get NO gluten. DH is sensitive to the tiniest amount of gluten. Personally, I don't take any chances at all! You couldn't drag me out to eat --- not unless it was a totally gluten-free restaurant. I don't eat anything that is not certified gluten-free or has not been tested. 99% of all we (hubs & I) eat are whole foods.

Do a lot of reading on here & you will learn much.

Sending you hugs (((()))))

Yikes! Hearing that I am most likely in for the long haul is not news that I really wanted to hear! But, I must admit that it does help somewhat when I have a clear idea of what to expect - it kind of takes the mystery out of things. Two to ten years seems like a very long time to be suffering but, in a strange sort of way it is comforting to know that there might actually be a light at the end of a very long tunnel. I just wish I had more support from the medical profession! :/ But, this forum has been hugely helpful and, I thank all of you for your honesty and support and also, for your sharing of knowledge, experiences, and wisdom. It really helps take the edge off things and, I don't feel as if I am alone suffering through all this hell.

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MO, I know. Me too. And if I weren't absolutely, positively sure that I am NOT getting gluten anywhere then I would be thinking that I had gotten cc'd. But this is what this stuff does.

If the docs say you're getting gluten from somewhere then ask them to do a celiac blood panel on you. If it comes up positive they are right ---- negative & they'll shut up.

Like you, the cooking....... it seems the hubs & my life centers each day around what's for breakfast, lunch, dinner. If we want to go anywhere it's all got to be planned around time to be home to cook our next meal which means we don't get much time out at all. We are trying to house hunt & it's damned hard to schedule showings around our cooking & eating. Someone always wants to make the showing around 10 or 11 b/c of their schedule & we have to worry if we will have time to see the place & drive back home. We do take snacks with us but still.......

Watch those band aids ..... they can cause dh places to form. I use them very judiciously these days. Hubs can't have a band aid on him anywhere.

Can you believe it?! When I went to the dermatologist in December, she did a biopsy but did the surgery smack dab on a spot where I had the most severe rash! :o/ I wish I had known at that time, that this was not acceptable! Then, she almost planted one of those Elastoplast bandages on the wound! I looked her straight in the eye and told her that the only thing my skin might tolerate is a piece of gauze and paper tape and that if she put that horrible bandage on me, my skin would break out big-time! What on earth was she thinking?!?! Where did some of these so-called dermatologists get their training, for heaven's sakes!! :(

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Itch, Here is some info. for you. You could print it out & take it to the next derm. There is a drug called Dapsone which keeps the dh from presenting. Many of us choose not to use it. Research before you do. Some of us can't use it.

And if you're gluten-free then none of the tests will come up positive.

IgA antibodies must be present in the skin biopsy for a definite diagnosis (4). It is important the person continues to eat gluten as the gluten-free diet can cause false negative results.

The NICE guideline on the recognition and diagnosis of coeliac disease recommends that people with DH should be screened for coeliac disease. The gastrointestinal symptoms of coeliac disease can be mild and in some cases are not apparent at all. Less than 10% of people with DH have gastrointestinal symptoms characteristic of coeliac disease (1).

Clinically, 10-20% of patients with DH present with classic symptoms of malabsorption and another 20% are estimated to have atypical symptoms, but at least 60% of patients have 'silent' coeliac disease.

The presence of DH is a marker of coeliac disease that is independent of the severity of histologic coeliac disease or the intestinal symptoms.

http://www.coeliac.o...s-herpetiformis

And this entire article is interesting & really should be read in it's entirety as it relates to both celiac disease & dh. Read especially, the last 1/3 of it. And it will verify much of what I stated.

http://www.ncbi.nlm....les/PMC2193738/

A novel hypothesis of autoimmune pathogenesis of

celiac disease consists of deamidation of wheat gliadin

by tissue transglutaminase, binding to HLA-DQ2 and

its recognition by gut T cells with subsequent production of epithelial damaging cytokines, matrix degrading

enzymes, and also IgA autoantibodies against tissue

transglutaminase.

12–14

In DH, a clinically silent but immunologically active celiac, disease in the gut could

produce IgA antibodies crossreacting with the connective tissue in the skin, a hypothesis presented already

for 30 years ago.

15

In contrast to the major progress

made in the characterization of the target antigens in

various autoimmune blistering disorders, such as pemphigus, pemphigoid, and linear IgA disease, one of the

main goals in the research on DH is still to resolve the

enigma of IgA deposition in the skin, what is the antigen, and does IgA have any role in blister formation.

Small Intestine

The occurrence of small intestinal mucosal abnormality

in DH was first reported in 1966, and shortly thereafter

it was recognized as gluten-sensitive and indistinguishable from ordinary celiac disease.

5,75

To date, it can be

concluded that all children and adults with DH have

celiac disease though most of the patients have no

gastrointestinal symptoms or signs of malabsorption.

7,18,77

The enteropathy in DH varies from flat mucosa to partial villous atrophy in about 75% of the

patients, and the remainder show minor morphological

changes and increased counts of intraepithelial lymphocytes.

7,18,27,57,76–78

At present, it is well established that

the patients with overt gastrointestinal symptoms represent only the top of the celiac iceberg and that there is

latent form of celiac disease showing only minor mucosal changes.

8,79

A certain population of intraepithelial

lymphocytes, CD4-, CD8-negative, gamma/delta T cell

receptor–bearing lymphocytes are closely associated

with celiac disease and DH.

33,80

The activation of these

gamma/delta T cells, exclusively found within epithelial tissues such as intestine and skin, seems to be

peptide and HLA independent.

81

Therefore, constant

presence of high numbers of gamma/delta T cells in the

epithelium of gluten-sensitive enteropathy suggests

that these cells have either a signaling function to immunocompetent cells or modulating function on epithelial cell growth.

Although the patients with DH have increased incidence of lymphoma and autoimmune diseases,

96

general mortality was not increased either in an English or

Finnish patient series.

During the last 30 years the research on DH has brought

up several important findings for dermatologists and

scientists. The change from a blistering dermatological

disease to a disorder in which both the skin and gut are

sensitive to cereal proteins, and also treatable by a GFD,

has been dramatic. The linkage to celiac disease revealed that DH is also a genetic disorder having a

strong association with HLA-DQ2 and a tendency to

cluster in families with celiac disease. Though granular

IgA deposits in dermal papillae are pathognomonic for

DH, and not present in the skin of patients with celiac

disease, their antigenic specificity remains to be elucidated in contrast to autoantibodies in the linear IgA

disease. The only circulating IgA autoantibody detected

to date in DH is the antibody against tissue transglutaminase. This antibody is, however, specific for glutensensitive enteropathy (i.e., for celiac disease), and it

may be involved together with DQ2-restricted, gliadinspecific T cell response in the pathogenesis of the gut

lesion. This novel hypothesis on the autoimmune

pathogenesis of gluten-sensitive enteropathy raises the

question if there is also a dermal autoantigen in DH

related to tissue transglutaminase.

http://suphu.medcom....rpetiformis.pdf

And there is this:

Role of gluten and association to coeliac disease

The first suggestion that patients with DH also have an enteropathy identical to coeliac disease (celiac disease) was made in 1967. This was confirmed by showing the enteropathy cleared with gluten withdrawal from the diet and recurred when gluten was reintroduced. It was subsequently shown that all patients with DH have evidence of a gluten enteropathy. However, in the majority of patients the enteropathy is mild and does not give rise to symptoms such as abdominal pain, weight loss and diarrhoea. Thus, all patients with DH have associated celiac disease although it could be described as latent celiac disease in the majority.

Diagnosis

The diagnosis of DH is made by a simple skin test. A small piece of skin approximately 3 mms in diameter is taken from an unaffected area, ie. normal looking skin. The skin is examined for the presence of a substance called IgA (immunoglobulin A) and is found at a specific site in the skin. Although the test is simple, it is important a laboratory experienced in the procedure undertakes the examination of the skin.

The diagnosis of DH can also be confirmed with the same tests as used for diagnosing celiac disease, ie. a small intestinal biopsy and blood tests looking for specific antibodies, called anti-endomysial and tissue transglutaminase antibodies. Occasionally in DH, the blood tests may be negative because their positivity correlates strongly with the severity of the intestinal lesion.

http://www.dermatiti...iformis.org.uk/

And then there is this one:

While DH is a known symptom of celiac, many patients with DH will not develop any classic digestive symptoms. This particular skin manifestation often does not correlate with a positive celiac diagnosis via biopsy. In fact, up to 20% of patients actually have normal small intestines when examined.

Some patients may exhibit signs of celiac, such as anemia or osteoporosis, at the time of their diagnosis.

How is it diagnosed?

o Skin Biopsy

o Misdiagnoses

While 70-80% of DH patients have higher than normal blood IgA- tTG antibody levels, a typical celiac panel (blood test) is not considered sufficient or reliable enough to properly diagnose patients.

Instead, doctors diagnose DH by examining the dermal papillae (cells under the top layer of skin), and use a process called direct immunofluorescence to detect for neutrophils and granular IgA deposits in the skin.

Granular IgA deposits (which indicate DH) appear in a very distinct pattern when inspected via immunofluorescence and appear in 98% of patients with DH - making it the gold standard in gaining a diagnosis.

These types of skin samples are collected by performing a biopsy, which involves incising tiny portions of unaffected skin positioned immediately next to reddened or blistered areas.

Inflammation and blistering of skin (likely caused by itching or scratching) can alter the look and concentration of the IgA deposits present in patients with DH, affecting the patient’s ability to receive a proper diagnosis. Because of this, it’s very important that unaffected skin be collected during a skin biopsy.

DH can often be misdiagnosed and frequently confused with skin conditions such as: allergies, bug or mosquito bites, contact dermatitis, diabetic pruritus, eczema, herpes, hives and psoriasis.

The lesioning of individual blisters can often lead to this misdiagnosis, as scarring can cause a change in presentation, making it difficult for doctors to differentiate DH from other skin conditions.

http://www.celiaccentral.org/skin/

http://www.ncbi.nlm....pubmed/17762854

Our data suggest that antibodies to eTG are the most sensitive serologic marker in treated and untreated patients with DH and confirm the central role of eTG in the pathogenesis of this disease. From:

http://www.ncbi.nlm....pubmed/19344979

The novel anti-GAF3X ELISA shows a higher sensitivity to detect celiac disease-associated autoantibodies in patients with DH compared with tests using nGli, tTG, or endomysium as substrates. From:

http://www.ncbi.nlm....pubmed/21840083

Virtually 100% of patients with DH have celiac disease, though the intestinal lesion is usually milder than most patients who have predominantly gastrointestinal complaints. The lesions of DH are very sensitive to even the ingestion of small amounts of gluten. Other dietary factors, for example iodine, may exacerbate the rash or prevent its healing. The rash is however dependant on the ingestion of gluten. While Dapsone will control the skin lesions of DH, a gluten-free diet allows Dapsone to be discontinued, healing of the intestine and reduction in the risk of the development of lymphoma that is increased in patients with DH. From:

http://www.celiacdis...rs/C02-What.htm

And from our own celiac.com:

With dermatitis herpetiformis the primary lesion is on the skin rather than the small intestine. The degree of damage to the small intestine is often less severe or more patchy then those with only celiac disease. Both diseases are permanent and symptoms/ damage will occur after comsuming gluten.

http://www.celiac.co...rmis/Page1.html

And from the Mayo Clinic:

http://www.mayomedic...terpretive/9360

"Circulating IgA endomysial antibodies (EMA) are present in 70% to 80% of patients with dermatitis herpetiformis or celiac disease, and in nearly all such patients who have high grade gluten-sensitive enteropathy and are not adhering to a gluten-free diet."

Cautions

A negative result (absence of circulating IgA-endomysial antibodies) does not exclude the diagnosis of dermatitis herpetiformis or celiac disease.

And from an article on celiac.com:

http://www.celiac.co...ults/Page1.html

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.

And from: http://www.arupconsu...mis.html#tabs=3

Celiac Disease Dual Antigen Screen with Reflex 2002026

Method: Semi-Quantitative Enzyme-Linked Immunosorbent Assay

Diagnose celiac disease in association with suspected or known dermatitis herpetiformis

Components include celiac disease dual antigen screen; tissue transglutaminase antibodies IgA and IgG; and gliadin peptide antibodies IgA and IgG

Monitor celiac disease and dermatitis herpetiformis during treatment

May be negative if patient is following a gluten-free diet

Some patients with dermatitis herpetiformis will also be negative

Monitor increased IgA endomysial and tissue transglutaminase antibodies

And from Medscape: http://emedicine.med.../1062640-workup

Serum markers, such as IgA endomysial antibodies, are negative in as many as 10-37% of patients with dermatitis herpetiformis.[28] Arguments have been made in favor of testing for tissue transglutaminase for diagnosis,[29] but tissue transglutaminase enzyme-linked immunosorbent assay positivity can occur in many autoimmune diseases because of impurities and cross-reactivity.[30]

The diagnosis is made after observing characteristic findings from skin biopsy specimens. The biopsy sample should be taken from the edge of a lesion for hematoxylin and eosin staining and from normal-appearing perilesional skin for direct immunofluorescence staining.

Results of direct immunofluorescence of lesional skin are often falsely negative. The vigorous immune response degrades the IgA antibody at the site. Therefore, biopsy specimens for the direct immunofluorescence studies should be taken from healthy-appearing skin.

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Itch, Here is some info. for you. You could print it out & take it to the next derm. There is a drug called Dapsone which keeps the dh from presenting. Many of us choose not to use it. Research before you do. Some of us can't use it.

And if you're gluten-free then none of the tests will come up positive.

IgA antibodies must be present in the skin biopsy for a definite diagnosis (4). It is important the person continues to eat gluten as the gluten-free diet can cause false negative results.

The NICE guideline on the recognition and diagnosis of coeliac disease recommends that people with DH should be screened for coeliac disease. The gastrointestinal symptoms of coeliac disease can be mild and in some cases are not apparent at all. Less than 10% of people with DH have gastrointestinal symptoms characteristic of coeliac disease (1).

Clinically, 10-20% of patients with DH present with classic symptoms of malabsorption and another 20% are estimated to have atypical symptoms, but at least 60% of patients have 'silent' coeliac disease.

The presence of DH is a marker of coeliac disease that is independent of the severity of histologic coeliac disease or the intestinal symptoms.

http://www.coeliac.o...s-herpetiformis

And this entire article is interesting & really should be read in it's entirety as it relates to both celiac disease & dh. Read especially, the last 1/3 of it. And it will verify much of what I stated.

http://www.ncbi.nlm....les/PMC2193738/

A novel hypothesis of autoimmune pathogenesis of

celiac disease consists of deamidation of wheat gliadin

by tissue transglutaminase, binding to HLA-DQ2 and

its recognition by gut T cells with subsequent production of epithelial damaging cytokines, matrix degrading

enzymes, and also IgA autoantibodies against tissue

transglutaminase.

12–14

In DH, a clinically silent but immunologically active celiac, disease in the gut could

produce IgA antibodies crossreacting with the connective tissue in the skin, a hypothesis presented already

for 30 years ago.

15

In contrast to the major progress

made in the characterization of the target antigens in

various autoimmune blistering disorders, such as pemphigus, pemphigoid, and linear IgA disease, one of the

main goals in the research on DH is still to resolve the

enigma of IgA deposition in the skin, what is the antigen, and does IgA have any role in blister formation.

Small Intestine

The occurrence of small intestinal mucosal abnormality

in DH was first reported in 1966, and shortly thereafter

it was recognized as gluten-sensitive and indistinguishable from ordinary celiac disease.

5,75

To date, it can be

concluded that all children and adults with DH have

celiac disease though most of the patients have no

gastrointestinal symptoms or signs of malabsorption.

7,18,77

The enteropathy in DH varies from flat mucosa to partial villous atrophy in about 75% of the

patients, and the remainder show minor morphological

changes and increased counts of intraepithelial lymphocytes.

7,18,27,57,76–78

At present, it is well established that

the patients with overt gastrointestinal symptoms represent only the top of the celiac iceberg and that there is

latent form of celiac disease showing only minor mucosal changes.

8,79

A certain population of intraepithelial

lymphocytes, CD4-, CD8-negative, gamma/delta T cell

receptor–bearing lymphocytes are closely associated

with celiac disease and DH.

33,80

The activation of these

gamma/delta T cells, exclusively found within epithelial tissues such as intestine and skin, seems to be

peptide and HLA independent.

81

Therefore, constant

presence of high numbers of gamma/delta T cells in the

epithelium of gluten-sensitive enteropathy suggests

that these cells have either a signaling function to immunocompetent cells or modulating function on epithelial cell growth.

Although the patients with DH have increased incidence of lymphoma and autoimmune diseases,

96

general mortality was not increased either in an English or

Finnish patient series.

During the last 30 years the research on DH has brought

up several important findings for dermatologists and

scientists. The change from a blistering dermatological

disease to a disorder in which both the skin and gut are

sensitive to cereal proteins, and also treatable by a GFD,

has been dramatic. The linkage to celiac disease revealed that DH is also a genetic disorder having a

strong association with HLA-DQ2 and a tendency to

cluster in families with celiac disease. Though granular

IgA deposits in dermal papillae are pathognomonic for

DH, and not present in the skin of patients with celiac

disease, their antigenic specificity remains to be elucidated in contrast to autoantibodies in the linear IgA

disease. The only circulating IgA autoantibody detected

to date in DH is the antibody against tissue transglutaminase. This antibody is, however, specific for glutensensitive enteropathy (i.e., for celiac disease), and it

may be involved together with DQ2-restricted, gliadinspecific T cell response in the pathogenesis of the gut

lesion. This novel hypothesis on the autoimmune

pathogenesis of gluten-sensitive enteropathy raises the

question if there is also a dermal autoantigen in DH

related to tissue transglutaminase.

http://suphu.medcom....rpetiformis.pdf

And there is this:

Role of gluten and association to coeliac disease

The first suggestion that patients with DH also have an enteropathy identical to coeliac disease (celiac disease) was made in 1967. This was confirmed by showing the enteropathy cleared with gluten withdrawal from the diet and recurred when gluten was reintroduced. It was subsequently shown that all patients with DH have evidence of a gluten enteropathy. However, in the majority of patients the enteropathy is mild and does not give rise to symptoms such as abdominal pain, weight loss and diarrhoea. Thus, all patients with DH have associated celiac disease although it could be described as latent celiac disease in the majority.

Diagnosis

The diagnosis of DH is made by a simple skin test. A small piece of skin approximately 3 mms in diameter is taken from an unaffected area, ie. normal looking skin. The skin is examined for the presence of a substance called IgA (immunoglobulin A) and is found at a specific site in the skin. Although the test is simple, it is important a laboratory experienced in the procedure undertakes the examination of the skin.

The diagnosis of DH can also be confirmed with the same tests as used for diagnosing celiac disease, ie. a small intestinal biopsy and blood tests looking for specific antibodies, called anti-endomysial and tissue transglutaminase antibodies. Occasionally in DH, the blood tests may be negative because their positivity correlates strongly with the severity of the intestinal lesion.

http://www.dermatiti...iformis.org.uk/

And then there is this one:

While DH is a known symptom of celiac, many patients with DH will not develop any classic digestive symptoms. This particular skin manifestation often does not correlate with a positive celiac diagnosis via biopsy. In fact, up to 20% of patients actually have normal small intestines when examined.

Some patients may exhibit signs of celiac, such as anemia or osteoporosis, at the time of their diagnosis.

How is it diagnosed?

o Skin Biopsy

o Misdiagnoses

While 70-80% of DH patients have higher than normal blood IgA- tTG antibody levels, a typical celiac panel (blood test) is not considered sufficient or reliable enough to properly diagnose patients.

Instead, doctors diagnose DH by examining the dermal papillae (cells under the top layer of skin), and use a process called direct immunofluorescence to detect for neutrophils and granular IgA deposits in the skin.

Granular IgA deposits (which indicate DH) appear in a very distinct pattern when inspected via immunofluorescence and appear in 98% of patients with DH - making it the gold standard in gaining a diagnosis.

These types of skin samples are collected by performing a biopsy, which involves incising tiny portions of unaffected skin positioned immediately next to reddened or blistered areas.

Inflammation and blistering of skin (likely caused by itching or scratching) can alter the look and concentration of the IgA deposits present in patients with DH, affecting the patient’s ability to receive a proper diagnosis. Because of this, it’s very important that unaffected skin be collected during a skin biopsy.

DH can often be misdiagnosed and frequently confused with skin conditions such as: allergies, bug or mosquito bites, contact dermatitis, diabetic pruritus, eczema, herpes, hives and psoriasis.

The lesioning of individual blisters can often lead to this misdiagnosis, as scarring can cause a change in presentation, making it difficult for doctors to differentiate DH from other skin conditions.

http://www.celiaccentral.org/skin/

http://www.ncbi.nlm....pubmed/17762854

Our data suggest that antibodies to eTG are the most sensitive serologic marker in treated and untreated patients with DH and confirm the central role of eTG in the pathogenesis of this disease. From:

http://www.ncbi.nlm....pubmed/19344979

The novel anti-GAF3X ELISA shows a higher sensitivity to detect celiac disease-associated autoantibodies in patients with DH compared with tests using nGli, tTG, or endomysium as substrates. From:

http://www.ncbi.nlm....pubmed/21840083

Virtually 100% of patients with DH have celiac disease, though the intestinal lesion is usually milder than most patients who have predominantly gastrointestinal complaints. The lesions of DH are very sensitive to even the ingestion of small amounts of gluten. Other dietary factors, for example iodine, may exacerbate the rash or prevent its healing. The rash is however dependant on the ingestion of gluten. While Dapsone will control the skin lesions of DH, a gluten-free diet allows Dapsone to be discontinued, healing of the intestine and reduction in the risk of the development of lymphoma that is increased in patients with DH. From:

http://www.celiacdis...rs/C02-What.htm

And from our own celiac.com:

With dermatitis herpetiformis the primary lesion is on the skin rather than the small intestine. The degree of damage to the small intestine is often less severe or more patchy then those with only celiac disease. Both diseases are permanent and symptoms/ damage will occur after comsuming gluten.

http://www.celiac.co...rmis/Page1.html

And from the Mayo Clinic:

http://www.mayomedic...terpretive/9360

"Circulating IgA endomysial antibodies (EMA) are present in 70% to 80% of patients with dermatitis herpetiformis or celiac disease, and in nearly all such patients who have high grade gluten-sensitive enteropathy and are not adhering to a gluten-free diet."

Cautions

A negative result (absence of circulating IgA-endomysial antibodies) does not exclude the diagnosis of dermatitis herpetiformis or celiac disease.

And from an article on celiac.com:

http://www.celiac.co...ults/Page1.html

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.

And from: http://www.arupconsu...mis.html#tabs=3

Celiac Disease Dual Antigen Screen with Reflex 2002026

Method: Semi-Quantitative Enzyme-Linked Immunosorbent Assay

Diagnose celiac disease in association with suspected or known dermatitis herpetiformis

Components include celiac disease dual antigen screen; tissue transglutaminase antibodies IgA and IgG; and gliadin peptide antibodies IgA and IgG

Monitor celiac disease and dermatitis herpetiformis during treatment

May be negative if patient is following a gluten-free diet

Some patients with dermatitis herpetiformis will also be negative

Monitor increased IgA endomysial and tissue transglutaminase antibodies

And from Medscape: http://emedicine.med.../1062640-workup

Serum markers, such as IgA endomysial antibodies, are negative in as many as 10-37% of patients with dermatitis herpetiformis.[28] Arguments have been made in favor of testing for tissue transglutaminase for diagnosis,[29] but tissue transglutaminase enzyme-linked immunosorbent assay positivity can occur in many autoimmune diseases because of impurities and cross-reactivity.[30]

The diagnosis is made after observing characteristic findings from skin biopsy specimens. The biopsy sample should be taken from the edge of a lesion for hematoxylin and eosin staining and from normal-appearing perilesional skin for direct immunofluorescence staining.

Results of direct immunofluorescence of lesional skin are often falsely negative. The vigorous immune response degrades the IgA antibody at the site. Therefore, biopsy specimens for the direct immunofluorescence studies should be taken from healthy-appearing skin.

Wow! Thanks so much for all this information, Squirmingitch! You have done an enormous amount of research! I am very impressed and also, very grateful! I am going to give it all a good read although, I suspect it will take some time to digest. It would seem that my derm definitely screwed up when she took the biopsy directly on the rash. And, seeing as I have been pretty much gluten-free since early December, I am deathly afraid of going back to eating gluten in order to increase the chances of getting accurate test results - assuming, of course, that the derm is even willing to do the tests! This recent flare is creating enough hell for me and, the mere thought of re-experiencing a rash virtually all over my body again - like I had it last fall - makes my blood run cold! As well, I believe Dapsone has sulpha in it and, I am sensitive to sulpha drugs - they make me break out in a dreadful rash and, that's all I need! More rashes! :o/ So, I doubt that I would be able to even consider the Dapsone route, even if I wanted to. I really appreciate all your help, Squirmingitch. You are totally awesome! Thanks. :o)

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YVW Itch. And I'm right there with you on so many avenues. No how, no way I am going back on gluten to prove to some doc something I already know! You put it well with "makes my blood run cold". Amen sister! Dapsone is in the sulfa class & I have problems with sulfamethoxozole. Despite this --- when I was out of my mind crazy insane with this latest flare --- I actually was ready to try it & damn the consequences! I'm finally healing & my mind is returning to more normal thinking.

 

There is (fourth down the line) a treatment using Tetracycline + niacinimide, however; I have not been able to find any info. as to how well it works or how long one has to continue on it or how rapidly it may work or anything at all --- not even what doses should be used.

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