Dermatitis herpetiformis (DH) is an autoimmune blistering disorder of known antibody IgA and unknown antigen associated with a gluten-sensitive enteropathy (GSE), and is generally accepted as a cutaneous manifestation of celiac disease and is characterized by grouped excoriations; erythematous, urticarial plaques; and papules with vesicles.
Dermatitis herpertiformis was also described as a Gell and Coombs local type III hypersensitivity reaction (Holgate and Church first edition). It is classically produced by gluten, but I have already seen to be produced by cow's milk.
May I suggest an immune modulator Internally. Fungi such as Ganoderma lucidum, or Hericium erinaceum, or the wood ear fungi Auricularia polytricha may produce this effect. Also a tree found here in North America known as Slippery Elm, it's bark has a mucilaginous consistency and can be gentle at repairing tissue both internally and externally.
Gliaden hypersensitivity. Gliaden is found in gluten (wheat, oat, rye, barely).
I have known that I have DH and have been gluten-free for 9 years. Spontaneous relapse can occur, so DH is likely due to disruption of the microbiome. In fact, the intestinal microbiota celiac patients is different from DH, with DH being similar to controls. Disruption of the intestinal barrier is theorized. In my personal experience, I am sensitive to milk after taking antibiotics. Complete removal of dairy from the diet for a month and slow re-introduction, presumably after the gut has "healed," returns my gut to a quiet state. I take probiotics as I do not seem to be able to sustain gut flora diversity without them. I eat a diet that is 75% whole, unprocessed foods. I also have about 10 food sensitivities that can produce migraine and GI symptoms. But none of the other foods trigger DH skin lesions. There is so much to learn and very little attention has been paid to other potential triggers of DH.
Wacklin P, Kaukinen K, Tuovinen E, et al. The duodenal microbiota composition of adult celiac disease patients is associated with the clinical manifestation of the disease. Inflammatory bowel diseases. 2013;19(5):934-941.
Some researchers have found in the gluten sensitive patients with DH that certain B cell receptors may act as antigen (they demonstrate it via various ex vivo and in vitro assays that are controversial as to their significance in the pathogenesis of the disease).
See :Br AND Wh, B CELL ANTIGENS IN GLUTEN SENSITIVE ENTEROPATHY AND DERMATITIS HERPETIFORMIS
DEAN L. MANN1, WARREN STROBER1, STEPHEN I. KATZ1, SHYUAN HSIA2, D. BERNARD AMOS2
1 National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
2 Division of Immunology, Duke University Medical Center, Durham, North Carolina 27710
Available online 16 June 2014
The Role of Products of the Histocompatibility Gene Complex in Immune Responses 1976, Pages 59–69
Sollid LM, Jabri B. Triggers and drivers of autoimmunity: lessons from coeliac disease. Nat Rev Immunol. Apr 2013;13(4):294-302.
Bana Jabri's lab at University of Chicago is doing some exciting work. This article is a great review on the possibilities of T cell and B cell mechanisms.
Dear all I am so pleased to hear from you may I add a study we had done for possible antigen and hear from you.
British Journal of Medicine & Medical Research
1(3): 163-169, 2011
SCIENCEDOMAIN international
www.sciencedomain.org
Dear Dr Bashir
I suggest its due to disturbance of the intestinal Floara , there is increase in the secretion of bacterial proteases which could have an antigentic effects.
I have studied allergens and autoantigen said in general and there is a common peptide sequence found in all that predisposes presentation. In the case of dermatitis, response to celiac transglutaminase, leads to a related response in thyroid, hair follicles and skin.
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