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Epidermolysis bullosa acquisita, also known as acquired epidermolysis bullosa, is a longterm autoimmune blistering skin disease. [1] It generally presents with fragile skin that blisters and becomes red with or without trauma. [2] Marked scarring is left with thin skin, milia and nail changes. [3] It typically begins around age 50. [2]
A coma blister, or coma bullae, is a skin lesion or blister that typically arises due to pressure in an individual with impaired consciousness. They vary in size, ranging from 4 to 5 centimeters in diameter, and may appear hemorrhagic or blood filled. [ 1 ]
Treatment of the epidermolysis bullosa by transplantation of laminin5 modified stem cells. Research has focused on changing the mixture of keratins produced in the skin. There are 54 known keratin genes—of which 28 belong to the type I intermediate filament genes and 26 to type II—which work as heterodimers. Many of these genes share ...
> 30% of the skin involved, skin biopsy [3] Differential diagnosis: Chickenpox, staphylococcal epidermolysis, staphylococcal scalded skin syndrome, autoimmune bullous disease [3] Treatment: Hospitalization, stopping the cause, pain medication [3] Prognosis: Mortality 20–50% [2] [3] Frequency: 1–2 per million per year (together with SJS) [2]
A vesiculobullous disease is a type of mucocutaneous disease characterized by vesicles and bullae (i.e. blisters).Both vesicles and bullae are fluid-filled lesions, and they are distinguished by size (vesicles being less than 5–10 mm and bulla being larger than 5–10 mm, depending upon which definition is used).
Epidermolysis bullosa simplex is caused by genetic mutations that prevent the proper formation of protein structures in the skin’s epidermis. The proteins of the outer epidermis do not bond properly with those of the inner dermis layer (dermal-epidermal junction).
The bullae are caused by exfoliative toxins produced by Staphylococcus aureus that cause the connections between cells in the uppermost layer of the skin to fall apart. [1] Bullous impetigo in newborns, children, or adults who are immunocompromised and/or are experiencing kidney failure, can develop into a more severe and generalized form ...
The bullae are formed by an immune reaction, initiated by the formation of IgG [citation needed] autoantibodies targeting dystonin, also called bullous pemphigoid antigen 1, [6] and/or type XVII collagen, also called bullous pemphigoid antigen 2, [7] which is a component of hemidesmosomes. A different form of dystonin is associated with ...