Dermatitis herpetiformis pathophysiology
|
Dermatitis herpetiformis Microchapters |
|
Differentiating Dermatitis herpetiformis from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Dermatitis herpetiformis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dermatitis herpetiformis pathophysiology |
|
Risk calculators and risk factors for Dermatitis herpetiformis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Dermatitis Herpetiformis (also called Duhring's disease), is a chronic itchy rash which is frequently associated with Celiac Disease. The rash is made of papules and vesicles which are present on different parts of the body mostly commonly on neck, trunk, buttocks and knees. It is an autoimmune mediated skin condition, which is IgA mediated reaction and is associated with gluten sensitivity of small bowel. There is presence of antibodies which leads to positive serology test results.
Dermatitis herpetiformis is associated with high prevalence of other autoimmune diseases.
Pathophysiology
Dermatitis herpetiformis is rare autoimmune skin condition which is strongly associated with celiac disease. The development of the rash is explained by both genetic and environmental factors which initiate the immune response.
Genetics
Dermatitis herpetiformis is found to be associated with the HLA DQ2 or HLA DQ8 alleles. The same alleles are found in patients with celiac disease, this explains the strong associated between celiac disease and dermatitis herpetiformis. The presence of these alleles in an individual presenting with symptoms of celiac disease or dermatitis herpetiformis has 100% negative predictive value.[1]
Environment
Gluten in diet is the most significant in the development of the skin rash. Gluten consists of Gliadin and Gutenin, bother are peptides. Gliadin is the one which is responsible for the pathogenesis of the disease.
Immune response
The rash is developed due to the body's immune response which causes inflammatory reaction on the skin. The antibodies formed against the antigen ' Gliadin' and the presence of other autoantibodies like transglutaminases, the later are the most important in the pathogenesis of the disease.
References
- ↑ Clarindo MV, Possebon AT, Soligo EM, Uyeda H, Ruaro RT, Empinotti JC. Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment. An Bras Dermatol. 2014;89(6):865-877. doi:10.1590/abd1806-4841.20142966