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Dh Flare Again.


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#16 GFreeMO

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Posted 28 January 2013 - 08:37 AM

Last night when I got in bed, DH was going crazy all over my butt cheeks..Now since I had breakfast, black coffee and rice with brown sugar it's going crazy on my shoulder blades. I can't stand this. It is making me so uncomfortable that I can not concentrate on anything.
Squirming, what kind of shampoo do you use? I've been using Suave lotion and shampoo and conditioner but I have DH on my scalp too now.
The gastro was no help at all with this.
Also, when the DH gets going, I get a fever which makes me feel like total crap.
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#17 squirmingitch

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Posted 28 January 2013 - 10:10 AM

MO, I use Suave Naturals for shampoo & conditioner --- they are gluten free.

I have noticed that when I eat, no matter what I'm eating I seem to get really itchy. I wonder if it has anything to do with leaky gut?

HUGS ((((MO))))
  • 0

Self diagnosed dh Sept. 2011~~~ confirmed dx July 18, 2012
Gluten free Dec. 2011
Soy free Dec. 2011
Hubs self diagnosed dh March 30, 2012
Hubs gluten free March 30, 2012

Summer 2013 We both have added back a little soy which is near unavoidable & we are doing okay with that small amount.

 


#18 GFreeMO

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Posted 28 January 2013 - 11:06 AM

Me too..same thing..Does not matter what I eat. You may be on to something with the leaky gut.

Ah well...I guess I just need to suck it up and deal with it.

I like Suave. It smells great!
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#19 squirmingitch

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Posted 28 January 2013 - 04:39 PM

I like Suave too. Smells great, works great & you can't beat the price. :)

I don't know about sucking it up..... it's pretty hard to suck this stuff up. :( :wacko:
  • 0

Self diagnosed dh Sept. 2011~~~ confirmed dx July 18, 2012
Gluten free Dec. 2011
Soy free Dec. 2011
Hubs self diagnosed dh March 30, 2012
Hubs gluten free March 30, 2012

Summer 2013 We both have added back a little soy which is near unavoidable & we are doing okay with that small amount.

 


#20 pricklypear1971

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Posted 31 January 2013 - 09:46 AM

Hey there honies,

So sorry to hear you're both having such a bad time.

After lots of reflection I figured out any sort of virus, illness would trigger DH in me (but my new flares were so much less than my old ones it was hard to figure it out). Quite frankly, it would trigger it more than iodine after 6-8 months gluten-free.

Anyway, one thing that helps dampen my AI symptoms is antihistimines. So, have either of you tried the different classes of antihistimines (Claritin being in one class, Alegra in another I believe). Check here for common OTC/classes: http://chronichives....information/#h1

If I am in an AI attack I have no qualms using 1/2 dose Children's Claritin every or every other day. It calms my AI reaction down.

That said, I'd try dapsone if I had DH like the two of you. Some people seem to take much longer to calm it down, and unfortunately it looks like y'all are in that category. I'm so sorry, I know it's miserable.
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Apparently there is nothing that cannot happen today. ~ Mark Twain

Probable Endometriosis, in remission from childbirth since 2002.
Hashimoto's DX 2005.
Gluten-Free since 6/2011.
DH (and therefore Celiac) dx from ND
.
Responsive to iodine withdrawal for DH (see quote, above).

Genetic tests reveal half DQ2, half DQ8 - I'm a weird bird!

#21 squirmingitch

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Posted 31 January 2013 - 10:18 AM

I have some Cyproheptadine 4 mg. tabs left over from pre-dx & I take 1/2 to start then 1/4 2 or 3 x per day & it helps with the itching but it certainly doesn't stop the itch & it does nothing else for the dh. Even though I always take them on a full stomach I find that after 3 days they begin to affect my stomach & I get burning indigestion.

Thanks Prickly for the tip. Will check it out.
  • 0

Self diagnosed dh Sept. 2011~~~ confirmed dx July 18, 2012
Gluten free Dec. 2011
Soy free Dec. 2011
Hubs self diagnosed dh March 30, 2012
Hubs gluten free March 30, 2012

Summer 2013 We both have added back a little soy which is near unavoidable & we are doing okay with that small amount.

 


#22 mendylou

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Posted 31 January 2013 - 01:34 PM

It was interesting to me to hear that someone else has the same issues with bandaids. In the past I would cover dhareas so I couldn't scratch the. As I removed the bandaid I would have the covered area now inflamed. I made my situation worse. My arms seemed to be the most sensitive. I only used bandaids on my legs & arms. Back & buttocks are almost impossible to reach, of course. My legs can tolerate the bandaids better than my arms, but don't leave on too long.
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#23 Itch Be Gone

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Posted 15 February 2013 - 07:38 PM

I had a horrible, itchy, burning rash over most of my body from early August to early December. A visit to a dermatologist was not at all helpful so, I decided to try a gluten-free diet to see if that might make a difference. Within a week, my rash was virtually gone and remained that way for 6 weeks while I continued with a very strict gluten-free diet. My digestion also improved, I had less joint pain and stiffness, and my nasal congestion improved as well. But, since mid-February, I have been having flare-ups - thankfully, not as bad as before I started on the gluten-free diet but, the rash is still red, raw, itchy, burning, and very uncomfortable - patches on my arms, chest, neck, face, back, and hips. Is this a common occurrence - to have nasty flare-ups like this even when I am on a strict gluten-free diet and even watching my iodine intake? I am starting to feel very discouraged, my nerves are getting a bit frayed, and I am feeling exhausted from having to go through this dreadful burning and itching again (all day and all night). Do I just need to be patient and trust that, over time, things will most likely improve as long as I stay true to this gluten-free diet? Or, am I most likely in for the long haul? I don't even know for sure if the rash is caused by gluten but, boy! It sure improved quickly after I dropped gluten from my diet! And, six whole weeks of being rash-free was total bliss! I even had smooth, soft skin for the first time in a very long time! But, now I am back to this hell and, for the life of me, I don't understand why this rotten, nasty rash has come back to haunt me! Any thoughts, suggestions etc. from any of you fellow sufferers "out there"?! Are flare-ups common? Does it ever get any better?!
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#24 mushroom

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Posted 15 February 2013 - 09:50 PM

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. :)
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Neroli


"Everything that can be counted does not necessarily count; everything that counts cannot necessarily be counted." - Albert Einstein

"Life is not weathering the storm; it is learning to dance in the rain"

"Whatever the question, the answer is always chocolate." Nigella Lawson

------------

Caffeine free 1973
Lactose free 1990
(Mis)diagnosed IBS, fibromyalgia '80's and '90's
Diagnosed psoriatic arthritis 2004
Self-diagnosed gluten intolerant, gluten-free Nov. 2007
Soy free March 2008
Nightshade free Feb 2009
Citric acid free June 2009
Potato starch free July 2009
(Totally) corn free Nov. 2009
Legume free March 2010
Now tolerant of lactose

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#25 squirmingitch

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Posted 16 February 2013 - 06:00 AM

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 (((()))))
  • 0

Self diagnosed dh Sept. 2011~~~ confirmed dx July 18, 2012
Gluten free Dec. 2011
Soy free Dec. 2011
Hubs self diagnosed dh March 30, 2012
Hubs gluten free March 30, 2012

Summer 2013 We both have added back a little soy which is near unavoidable & we are doing okay with that small amount.

 


#26 Itch Be Gone

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Posted 16 February 2013 - 04:33 PM

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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#27 Itch Be Gone

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Posted 16 February 2013 - 04:42 PM

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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#28 Itch Be Gone

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Posted 16 February 2013 - 06:11 PM

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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#29 squirmingitch

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Posted 16 February 2013 - 06:25 PM

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.
  • 0

Self diagnosed dh Sept. 2011~~~ confirmed dx July 18, 2012
Gluten free Dec. 2011
Soy free Dec. 2011
Hubs self diagnosed dh March 30, 2012
Hubs gluten free March 30, 2012

Summer 2013 We both have added back a little soy which is near unavoidable & we are doing okay with that small amount.

 


#30 Itch Be Gone

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Posted 16 February 2013 - 08:09 PM

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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