Erythroderma. Who, where, when, why, and how ..

Expression of VCAM‐1, ICAM‐1, E‐selectin, and P‐selectin on endothelium in situ in patients with erythroderma, mycosis fungoides and atopic dermatitis

“…Erythroderma may result from different causes, but at present it is still unclear whether the underlying patho-mechanisms that lead to erythroderma are identical or different depending on the original disease. [2][3][4] No data were available on adhesion molecule expression on endothelial cells in situ in erythroderma, but only some data on circulating adhesion molecules. Groves et al found significant elevated levels of circulating adhesion molecules ICAM-1, VCAM-1 and Eselectin in benign reactive erythroderma as compared to healthy controls.…”

“…2,3 What makes erythroderma intriguing is the fact that skin diseases, which are clinically totally different, can progress into erythroderma with a relatively uniform clinical picture. 4 T-helper lymphocytes are the most prominent cells in the skin infiltrate in erythroderma. 3,5,6 We have shown that the dermal infiltrate in patients with Sézary syndrome mainly express interleukin (IL)-4 (Th2 cytokine profile) in contrast to interferon (IFN)-g (Th1 cytokine profile) in benign reactive erythroderma.…”

Erythroderma: A Clinical Study of 127 Cases and Review of the Literature

“…In the study of Botella-Estrada et al [8], the best clinicohistological correlation was found in cutaneous-T-cell-lymphoma-related El Euch et al erythroderma. Biopsy specimens taken from sites of predilection of papulosquamous diseases that persist for more than 3-6 weeks after the erythema has resolved are more likely to have diagnostic features [15]. Only 1 patient in our series showed a malignant node infiltration revealing a CD30 T cell lymphoma not evident in previous skin biopsies.…”

Interleukin 4 and interferon‐γ expression of the dermal infiltrate in patients with erythroderma and mycosis fungoides. An immuno‐histochemical study

“…Erythroderma may result from different causes, but at present it is unclear whether the underlying pathomechanisms that lead to erythroderma are identical or different depending on the original disease. [1][2][3][4] Data are available on cytokine mRNA expression in skin of patients with Sézary syndrome but not on other types of erythroderma. These studies demonstrate a Th2 cytokine profile in Sézary syndrome.…”

“…At present it is unclear whether one ''final common patho-mechanism'', or multiple mechanisms lead to erythroderma. 4 T lymphocytes are the most prominent cells in skin infiltrate in erythroderma and mycosis fungoides, with CD4π cells outnumbering CD8π cells in most cases. 3,[5][6][7] In Sézary syndrome and also in mycosis fungoides, which both are cutaneous T-cell lymphomas, a malignant monoclonal proliferation of T cells is found in skin.…”