Immune System Changes in DH
The technique of using fluorescent staining of the skin reveals the accumulation of granular immunoglobin deposits in the dermal papillary tips. In dermatitis herpetiformis (DH) patients these deposits are found to be of the immunoglobulin class IgA. This diagnostic test greatly enhances the accuracy of the diagnosis of DH. It has been found that these deposits of IgA are present in normal skin as well as in skin near the lesions of DH. Conversely, these findings have not been detected in patients who do not have DH.
IgA is an antibody produced in the mucous membranes of the nose, throat, lungs and gut. IgA is produced by the body in response to foreign substances (antigens) which are breathed in or taken in with food. It is felt that this IgA activates a complement system in the body through what is called the alternate complement pathway. This system is the actual method whereby the damage is done or the inflammation is produced.
Theory of What Causes DH
There is within the immune system a genetically-based sensitivity to gluten. When gluten is in the diet, the body makes IgA. The IgA or the Iga-gluten (antigen-antibody) complex circulates in the blood stream. The IgA or the complex settles in the skin causing the intense reaction labeled dermatitis herpetiformis. It is not known why individuals with celiac disease do not also develop the skin rash and the DH symptoms.
The pathology of the gluten-sensitive enteropathy (GSE) associated with DH and that in ordinary GSE (celiac disease) are essentially the same, although the lesions in the jejunum (12- to 14-inch section of the small intestine) in ordinary GSE (celiac disease) are usually much more severe. It is important to note that lesions in the jejunum for both dermatitis herpetiformis and celiac disease in no way represent the skin lesions of DH and that the IgA deposits are not found around the lesions in the gut membranes. Most patients with DH are symptom-free as far as the gastrointestinal tract is concerned; only 14 to 20 percent of patients with DH have malabsorption of fat, D-Xylose, or iron, or any combination as is typical of patients with GSE (celiac disease).
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