I made a post on another thread in the post dx forum & some there were saying they did not know much about dh 7 wouldn't mind learning more as well as wanting to know what the source was for things I stated. Here is my post, copied & pasted. I did not want to hijack the other thread plus this forum is the best place to discuss dh so I post the sources here.
My post from http://www.celiac.com/gluten-free/topic/95135-my-biopsy-word-for-word/page__st__30
I will also add a tidbit of information here. In the case of celiacs with dermatitis herpetiformis; we test negative on the blood panel even more often than celiacs with the GI issues. We also have patchier damage in the gut so it's harder to find with an endoscopy/biopsy. Thus, it's even more difficut for us to get an "official" dx. We can have the area adjacent to a lesion biopsied but we have to have been actively eating gluten just like for the blood panel & endoscopy PLUS there is a 37% false negative return on the biopsy. AND you had better have a derm who REALLY knows their stuff doing the biopsy. All in all; it's harder than heck to get a dyed in the wool dx.
Now, here are the sources along with selected excerpts:
DH is diagnosed by a skin biopsy. Biopsy needs to be performed on uninvolved skin (clinically normal-appearing skin immediately next to an area of inflammation). False negatives may occur if a biopsy is performed on skin that is affected by the condition.
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.org.uk/healthcare-professionals/associated-conditions-and-complications/dermatitis-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.nih.gov/pmc/articles/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.
1214
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.
7,18,27,57,7678
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
receptorbearing 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.ch/uploads/media/Dermatitis_herpetiformis.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.dermatitisherpetiformis.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 patients ability to receive a proper diagnosis. Because of this, its 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.nih.gov/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.nih.gov/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.nih.gov/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.celiacdiseasecenter.org/C_Doctors/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.com/articles/177/1/The-Gluten-Intolerance-Group-of-North-America-on-Iodine-and-Dermatitis-Herpetiformis/Page1.html
And from the Mayo Clinic:
http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/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.com/articles/57/1/Interpretation-of-Celiac-Disease-Blood-Test-Results/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.arupconsult.com/Topics/DermHerpetiformis.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.medscape.com/article/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.
My post from http://www.celiac.com/gluten-free/topic/95135-my-biopsy-word-for-word/page__st__30
I will also add a tidbit of information here. In the case of celiacs with dermatitis herpetiformis; we test negative on the blood panel even more often than celiacs with the GI issues. We also have patchier damage in the gut so it's harder to find with an endoscopy/biopsy. Thus, it's even more difficut for us to get an "official" dx. We can have the area adjacent to a lesion biopsied but we have to have been actively eating gluten just like for the blood panel & endoscopy PLUS there is a 37% false negative return on the biopsy. AND you had better have a derm who REALLY knows their stuff doing the biopsy. All in all; it's harder than heck to get a dyed in the wool dx.
Now, here are the sources along with selected excerpts:
DH is diagnosed by a skin biopsy. Biopsy needs to be performed on uninvolved skin (clinically normal-appearing skin immediately next to an area of inflammation). False negatives may occur if a biopsy is performed on skin that is affected by the condition.
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.org.uk/healthcare-professionals/associated-conditions-and-complications/dermatitis-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.nih.gov/pmc/articles/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.
1214
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.
7,18,27,57,7678
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
receptorbearing 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.ch/uploads/media/Dermatitis_herpetiformis.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.dermatitisherpetiformis.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 patients ability to receive a proper diagnosis. Because of this, its 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.nih.gov/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.nih.gov/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.nih.gov/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.celiacdiseasecenter.org/C_Doctors/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.com/articles/177/1/The-Gluten-Intolerance-Group-of-North-America-on-Iodine-and-Dermatitis-Herpetiformis/Page1.html
And from the Mayo Clinic:
http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/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.com/articles/57/1/Interpretation-of-Celiac-Disease-Blood-Test-Results/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.arupconsult.com/Topics/DermHerpetiformis.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.medscape.com/article/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.