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Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment.

Clarindo MV, Possebon AT, Soligo EM, Uyeda H, Ruaro RT, Empinotti JC - An Bras Dermatol (2014 Nov-Dec)

Bottom Line: These lesions are vesico-bullous, pruritic, and localized especially on elbows, knees and buttocks, although atypical presentations can occur.Immunofluorescence of perilesional area is considered the gold standard for diagnosis, but serological tests help in cases where it is negative.Dapsone remains the main drug for treatment, but it requires monitoring of possible side effects, some potentially lethal.

View Article: PubMed Central - PubMed

Affiliation: West ParanĂ¡ State University, Cascavel, PR, Brazil.

ABSTRACT
Researches on DH have shown that it is not just a bullous skin disease, but a cutaneous-intestinal disorder caused by hypersensitivity to gluten. Exposure to gluten is the starting point of an inflammatory cascade capable of forming autoantibodies that are brought to the skin, where they are deposited, culminating in the formation of skin lesions. These lesions are vesico-bullous, pruritic, and localized especially on elbows, knees and buttocks, although atypical presentations can occur. Immunofluorescence of perilesional area is considered the gold standard for diagnosis, but serological tests help in cases where it is negative. Patients who follow gluten-free diets have better control of symptoms on the skin and intestine, as well as lower risks of progression to lymphoma. Dapsone remains the main drug for treatment, but it requires monitoring of possible side effects, some potentially lethal.

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Related in: MedlinePlus

Dermatitis Herpetiformis physiopathogenesis
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f01: Dermatitis Herpetiformis physiopathogenesis

Mentions: Sardy et al first described ETG in 2002.21 It is present in keratinocytes andamong its functions we highlight the maintenance of stratum corneum's integrity.Also known as transglutaminase 3, it performs its function by connecting thevarious epidermal structural proteins.22 TTG is the main antigen for CD antibodies, as ETG is theantigen in DH. Anti-TTG antibodies may, by cross-reaction, recognize ETG, leadingto the onset of cutaneous IgA deposits (Figure1). Between TTG and ETG molecules there is 64% structural homology,which would explain the occurrence of cross-reaction. Serum from patients with CDreact against TTG and ETG, whilst those of patients with DH react mainly againstETG.21,23-26


Dermatitis herpetiformis: pathophysiology, clinical presentation, diagnosis and treatment.

Clarindo MV, Possebon AT, Soligo EM, Uyeda H, Ruaro RT, Empinotti JC - An Bras Dermatol (2014 Nov-Dec)

Dermatitis Herpetiformis physiopathogenesis
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230654&req=5

f01: Dermatitis Herpetiformis physiopathogenesis
Mentions: Sardy et al first described ETG in 2002.21 It is present in keratinocytes andamong its functions we highlight the maintenance of stratum corneum's integrity.Also known as transglutaminase 3, it performs its function by connecting thevarious epidermal structural proteins.22 TTG is the main antigen for CD antibodies, as ETG is theantigen in DH. Anti-TTG antibodies may, by cross-reaction, recognize ETG, leadingto the onset of cutaneous IgA deposits (Figure1). Between TTG and ETG molecules there is 64% structural homology,which would explain the occurrence of cross-reaction. Serum from patients with CDreact against TTG and ETG, whilst those of patients with DH react mainly againstETG.21,23-26

Bottom Line: These lesions are vesico-bullous, pruritic, and localized especially on elbows, knees and buttocks, although atypical presentations can occur.Immunofluorescence of perilesional area is considered the gold standard for diagnosis, but serological tests help in cases where it is negative.Dapsone remains the main drug for treatment, but it requires monitoring of possible side effects, some potentially lethal.

View Article: PubMed Central - PubMed

Affiliation: West ParanĂ¡ State University, Cascavel, PR, Brazil.

ABSTRACT
Researches on DH have shown that it is not just a bullous skin disease, but a cutaneous-intestinal disorder caused by hypersensitivity to gluten. Exposure to gluten is the starting point of an inflammatory cascade capable of forming autoantibodies that are brought to the skin, where they are deposited, culminating in the formation of skin lesions. These lesions are vesico-bullous, pruritic, and localized especially on elbows, knees and buttocks, although atypical presentations can occur. Immunofluorescence of perilesional area is considered the gold standard for diagnosis, but serological tests help in cases where it is negative. Patients who follow gluten-free diets have better control of symptoms on the skin and intestine, as well as lower risks of progression to lymphoma. Dapsone remains the main drug for treatment, but it requires monitoring of possible side effects, some potentially lethal.

Show MeSH
Related in: MedlinePlus