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Because EDP is an uncommon disease of the skin, it is important to consider other skin diseases that may resemble erythema dyschromicum perstans, such as infectious diseases (i.e. leprosy or pinta), reaction to drugs, post inflammatory hyperpigmentation, or lichen planus pigmentosus. There is no cure for EDP.
Positive epidermal side staining by indirect immunofluorescence microscopy on human salt-split skin (IIF SSS) on a serum sample. Not otherwise specified [notes 2] A lesion with superficial lymphoeosinophilic infiltrate without additional histopathologic characteristics can be due to for example drug reactions and insect bites. [2] [notes 2]
Psoriatic erythroderma can be congenital or secondary to an environmental trigger. [12] [13] [14] Environmental triggers that have been documented include sunburn, skin trauma, psychological stress, systemic illness, alcoholism, drug exposure, chemical exposure (e.g., topical tar, computed tomography contrast material), and the sudden cessation of medication.
Xanthoerythrodermia perstans is a distinct variant with lesions that are yellow in color. [ 1 ] [ 2 ] : 452 Digitate dermatosis is a distinct variant with lesions in the shape of a finger and distributed symmetrically on the flanks.
Erythema annulare centrifugum (EAC), is a descriptive term for a class of skin lesion [2] presenting redness in a ring form (anulare) that spreads from a center (centrifugum). It was first described by Darier in 1916.
Postinflammatory hyperpigmentation (PIH) is a skin condition characterized by the darkening of the skin (hyperpigmentation) following an inflammatory injury, such as acne, dermatitis, infectious disease, or trauma.
Erythema (Ancient Greek: ἐρύθημα, from Greek erythros 'red') is redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries. [1] It occurs with any skin injury, infection, or inflammation .
Psoriasis is a cellular autoimmune reaction caused by T-cells to what are thought to be skin-resident self-antigens. [3] The psoriasiform reaction is brought on by an increase in interferon-γ and interleukin-17, which interact with mast cells, neutrophils, macrophages, and dermal cells. [4]