dermatitis herpetiformis/protease

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A rare case of dermatitis herpetiformis requiring parenteral heparin for long-term control.

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We report a patient with controlled coeliac disease but severe dermatitis herpetiformis who was intolerant of dapsone and sulphapyridine. She ultimately had to be treated with parenteral heparin which brought about involution of the skin lesions with symptomatic relief within 1 week. The mechanism

Mast cells in developing subepidermal bullous diseases: emphasis on tryptase, chymase and protease inhibitors.

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The possible involvement of mast cell tryptase and chymase in subepidermal bullous diseases was studied enzyme-histochemically in specimens from erythematous and vesicular skin and from non-involved skin of patients with dermatitis herpetiformis, bullous pemphigoid, erythema multiforme, infective

Expression of Elafin in Dermatitis Herpetiformis.

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BACKGROUND Elafin is a serine protease inhibitor that has various epithelial cell regulatory and immunomodulatory effects including inactivation of neutrophil elastases. This later role originated the interest of elafin in certain neutrophil-rich dermatoses. Interestingly, it has been speculated

Induction of lesions of dermatitis herpetiformis by autologous serum.

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In the present study various factors which contribute to the initiation of lesions in dermatitis herpetiformis (DH) were examined. Thirty-one patients with DH, seven with bullous pemphigoid, two with linear IgA disease and two healthy subjects were studied either before starting treatment or after

Gene expression profiling in dermatitis herpetiformis skin lesions.

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Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy

Autoimmunity-driven enzymatic remodeling of the dermal-epidermal junction in bullous pemphigoid and dermatitis herpetiformis.

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Pathogenesis of blister formation in bullous pemphigoid (BP) and dermatitis herpetiformis (DH) is associated with destruction of numerous components of the dermal--epidermal junction. Proteolytic enzymes (PE) are involved in a multitude of physiological reactions and may have impact on the

Demonstration of collagenase and elastase activities in the blister fluids from bullous skin diseases. Comparison between dermatitis herpetiformis and bullous pemphigoid.

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We have investigated potential mechanisms for blister formation by assaying proteolytic enzymes in the blister fluids of patients with various bullous diseases. Blister fluids were obtained from patients with dermatitis herpetiformis (DH), bullous pemphigoid (BP), chronic bullous disease of

Granzyme B is elevated in autoimmune blistering diseases and cleaves key anchoring proteins of the dermal-epidermal junction.

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In healthy skin, epidermis and dermis are anchored together at the dermal-epidermal junction (DEJ), a specialized basement membrane pivotal for skin integrity and function. However, increased inflammation in the DEJ is associated with the disruption and separation of this junction and sub-epidermal

The Value of Direct Immunofluorescence on Proteinase-Digested Formalin-Fixed Paraffin-Embedded Skin Biopsies.

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Direct immunofluorescence (DIF) on frozen tissue (DIF-F) is the method of choice for the identification of immune deposits present in skin and other tissues. DIF can also be performed on formalin-fixed paraffin-embedded tissue (DIF-P) after antigen retrieval with proteases and has proven to be of

[Autoimmune pemphigus combined with alpha 1-antitrypsin deficiency].

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It has been demonstrated experimentally that the bullae observed in autoimmune pemphigus are due to the action of proteases. So far, no case of pemphigus associated with deficiency in antiprotease has been reported. We present a case of pemphigus associated with familial deficiency in alpha

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