Dermatitis Herpetiformis – Some Important Facts You Should Know

The Dermatitis Herpetiformis which is also known as DH is an exquisitely pruritic eruption. With more emphasis, it is majorly seen on the buttocks and on the surfaces of the arms and legs. Other severe cases may involve larger surface areas.

Also, the Dermatitis Herpetiformis is a chronic blistering skin condition. It is characterized by blisters which if filled with a watery fluid.

DH (Dermatitis Herpetiformis) is not in any way related nor caused by herpes virus. From the name it simply means a skin inflammation which have the appearance similar to herpes.

Louise Adolphus Duhiring was the first person who described dermatitis herpetiformis, in the year 1884. Also the connection between celiac disease and DH was formally recognized in 1967.

Meanwhile, the DH is a specific manifestation of coeliac disease. In addition to that, the exact mechanism is not known.

Men and women are affected equally. The age of this disease is about 15 to 40, so this is capable of children and the elderly also.

The estimates of dermatitis herpetiformis on face prevalence vary from 1 in 400 to 1 in 10,000. It is most common in patients of northern European/northern Indian ancestry, and is associated with the human leukocyte antigen (HLA) haplotype HLA-DQ2 along with coeliac disease and gluten sensitivity.

More Facts About Dermatitis Herpetiformis

DH is super characterized by intensely itchy, chronic papulovesicular eruptions. The blisters have different and several sizes.

The infected surfaces could be the face, scalp, back, hairline, groin, back of neck, the buttocks etc.

Unlike the mesothelioma cancer, the dermatitis herpetiformis symptoms usually appear in the early years of adulthood (20 to 30 years of age).

This condition (DH) is very itchy that you will scratch to the level of even rubbing off your buttocks. This itching condition makes the diseased to even forget the fact that he needs to consult a doctor.

The torments of this disease varies depending on the amount of gluten which was ingested. Now in terms of pathology, the first signs of this condition may observed withing the dermis.

However this changes may probably take place at this levels which includes Vascular Dilatation, Edema and Cellular Infiltration. This is commonly for eosinophils and lymphocytes.

Meanwhile various research studies have pointed out at different potential factors that may play a larger or smaller role in the development of dermatitis herpetiformis.

Ideally the bullae which is found in the skin affected by dermatitis herpetiformis are subepidermal and have rounded lateral borders.

The fact that eTG has been found in precipitates of skin-bound IgA from skin affected by this condition has been used to conclude that dermatitis herpetiformis may be caused by a deposition of both IgA and eTG within the dermis.

It is estimated that these deposits may resorb after ten years of following a gluten-free diet. Moreover, it is suggested that this condition is closely linked to genetics.

This theory is based on the arguments that individuals with a family history of gluten sensitivity who still consume foods containing gluten are more likely to develop the condition as a result of the formation of antibodies to gluten.

These antibodies cross-react with eTG, and IgA/eTG complexes deposit within the papillary dermis to cause the lesions of dermatitis herpetiformis.

These IgA deposits may disappear after long-term (up to ten years) avoidance of dietary gluten.

Dermatitis herpetiformis may be characterised based on inflammation in the skin and gut. Inflammation in the gut is similar to, and linked to, celiac disease.

tTG is treated as an autoantigen, especially in people with certain HLA-DQ2 and HLA-DQ8 alleles and other gene variants that cause atopy. tTG is up-regulated after gluten absorption. cDCs endocytose tTG-modified gliadin complexes or modified gliadin alone but they only present gliadin to CD4+ T cells on pMHC-II complexes. These T cells become activated and polarised into type I helper T (Th1) cells. Th1 cells reactive towards gliadin have been discovered, but none against tTG.

Meanwhile, a naive B cell sequesters tTG-modified gliadin complexes from the surface of cDCs in the lymph nodes(LNs) before they become endocytosed by the cDCs.

The B cell receptor (membrane bound antibody; BCR) is specific to the tTG portion of the complex. The B cell endocytoses the complex and presents the modified gliadin to the activated Th1 cell’s T cell receptor (TCR) via pMHC-II in a process known as epitope spreading.

Thus, the B cell presents the foreign peptide (modified gliadin) but produces antibodies specific for the self-antigen (tTG).

Once the B cell becomes activated, it differentiates into plasma cells that secrete autoantibodies against tTG, which may be cross-reactive with epidermal transglutanimase (eTG).

Class A antibodies (IgA) deposit in the gut. Some may bind to the CD89 (FcαRI) receptor on macrophages (M1) via their Fc region (constant region). This will trigger endocytosis of the tTG-IgA complex, resulting in the activation of macrophages. Macrophages secrete more IL-8, propagating the neutrophil-mediated inflammatory response.

The purportedly cross-reactive autoantibodies may migrate to the skin in dermatitis herpetiformis. IgA deposits may form if the antibodies cross-react with epidermal transglutanimase (eTG).

Some patients have eTG-specific antibodies instead of tTG-specific cross-reactive antibodies and the relationship between dermatitis herpetiformis and celiac disease in these patients is not fully understood.

Macrophages may be stimulated to secrete IL-8 by the same process as is seen in the gut, causing neutrophils to accumulate at sites of high eTG concentrations in the dermal papillae of the skin.

Neutrophils produce pus in the dermal papillae, generating characteristic blisters. IL-31 accumulation at the blisters may intensify itching sensations. Memory B and T cells may become activated in the absence of PAMPs and DAMPs during successive encounters with tTG-modified gliadin complexes or modified gliadin alone, respectively. Symptoms of dermatitis herpetiformis are often resolved if patients avoid a gluten-rich diet.

Dermatitis Herpetiformis Symptoms

Dermatitis herpetiformis symptoms often are misdiagnosed, being confused with drug eruptions, contact dermatitis, dishydrotic eczema (dyshidrosis), and even scabies.

Having known all these, it is very essential that you take precautions so as to avoid being infected with this. Remember that the DH is very deadly just like every other diseases you can mention.

There are diseases like mesothelioma and asbestos related cancers which seem to be deadly just like this DH.

So having read this, did you find this content very resourceful? do you have any question to ask? and what’s your take on this?

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