Sigurdsson V, de Vries I J, Toonstra J, Bihari I C, Thepen T, Bruijnzeel-Koomen C A, van Vloten W A
Department of Dermatology and Allergology, University Medical Center Utrecht, The Netherlands.
J Cutan Pathol. 2000 Oct;27(9):436-40. doi: 10.1034/j.1600-0560.2000.027009436.x.
Erythroderma may result from different causes. At present it is unclear whether the patho-mechanisms that lead to these different types of erythroderma are identical or different. Adhesion molecules and their ligands play a major role in endothelial-leukocyte interactions, which affect the binding, transmigration and infiltration of lymphocytes and mononuclear cells during inflammation, injury, or immunological stimulation. The aim of this study was to investigate the adhesion molecule expression on endothelial cells in erythroderma in situ.
Snap-frozen skin biopsy specimens from 23 patients with erythroderma were studied. Eight had idiopathic erythroderma, 5 erythrodermic atopic dermatitis, 4 Sézary syndrome and 6 had erythroderma from miscellaneous causes. As a control we studied skin specimens from 10 patients with mycosis fungoides, 5 patients with atopic dermatitis and 5 healthy non-atopic volunteers. To determine adhesion molecule expression on endothelial cells in situ, sections were immuno-histochemically double stained with biotinylated Ulex Europaeus agglutinin 1 as a pan-endothelial cell marker, and for the adhesion molecules VCAM-1, ICAM-1, E-, and P-selectin. All double- and single-stained blood vessels in the dermis were counted.
Mean endothelial expression in erythroderma was as follows: VCAM-1 51.4%, ICAM-1 70.1%, E-selectin 43.5%, and P-selectin 52.6%. There was no statistical difference between different groups of erythroderma. Mean expression of all adhesion molecules tested, was in Sézary syndrome higher than in mycosis fungoides albeit not significant. In erythrodermic atopic dermatitis only VCAM-1 expression was significantly higher than in lesional skin of atopic dermatitis. No differences were observed in expression of the other three adhesion molecules.
There is no difference regarding adhesion molecule expression on endothelial cells between different types of erythroderma.
红皮病可能由多种原因引起。目前尚不清楚导致这些不同类型红皮病的病理机制是相同还是不同。黏附分子及其配体在内皮细胞与白细胞的相互作用中起主要作用,在炎症、损伤或免疫刺激过程中影响淋巴细胞和单核细胞的黏附、迁移和浸润。本研究的目的是原位研究红皮病内皮细胞上黏附分子的表达情况。
对23例红皮病患者的皮肤活检速冻标本进行研究。其中8例为特发性红皮病,5例为红皮病型特应性皮炎,4例为 Sézary 综合征,6例为其他原因引起的红皮病。作为对照,我们研究了10例蕈样肉芽肿患者、5例特应性皮炎患者和5名健康非特应性志愿者的皮肤标本。为了原位确定内皮细胞上黏附分子的表达,切片用生物素化的欧洲荆豆凝集素1作为全内皮细胞标记物进行免疫组织化学双重染色,并检测黏附分子 VCAM-1、ICAM-1、E-选择素和 P-选择素。对真皮中所有双重和单染色的血管进行计数。
红皮病中内皮细胞的平均表达如下:VCAM-1 为51.4%,ICAM-1 为70.1%,E-选择素为43.5%,P-选择素为52.6%。不同类型的红皮病之间无统计学差异。在 Sézary 综合征中,所有检测的黏附分子的平均表达均高于蕈样肉芽肿,尽管差异不显著。在红皮病型特应性皮炎中,仅 VCAM-1 的表达显著高于特应性皮炎的皮损。其他三种黏附分子的表达未观察到差异。
不同类型红皮病在内皮细胞上的黏附分子表达无差异。