ABSTRACT
BACKGROUND: The migration of circulating monocytes into the dermis is considered to be essential for both the initiation and the progression of xanthoma. The contribution of vascular endothelial cells to the migration process is unclear. METHODS: Twenty cases of xanthelasma and six cases of tuberous xanthoma lesions were analyzed using immunohistochemical staining. RESULTS: Xanthoma lesions contained up to 25-fold more von Willebrand factor-stained endothelial cells than normal skin. The prevalence of E-selectin-positive endothelial cells increased by up to threefold more in xanthoma lesions than in normal skin. In contrast, the prevalence of intercellular cell adhesion molecule-1 (ICAM-1) decreased up to 3.5-fold more in xanthoma lesions than in normal skin. In xanthoma lesions, almost all ICAM-1-positive endothelial cells co-expressed with E-selectin but many endothelial cells, which only expressed E-selectin, were also found in the lesions and the ratio of macrophages to endothelial cells was higher (10:1) than that in normal skin (5:1). CONCLUSIONS: Endothelial cells proliferate and express E-selectin rather than ICAM-1 under a microenvironment in which macrophages predominate rather than endothelial cells, thereby promoting macrophage migration into xanthoma lesions.
Subject(s)
Cell Adhesion Molecules/metabolism , Endothelial Cells/pathology , Skin Diseases/pathology , Xanthomatosis/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Biomarkers/metabolism , Cell Count , Cell Movement , Dermis/metabolism , Dermis/pathology , E-Selectin/metabolism , Endothelial Cells/metabolism , Female , Fluorescent Antibody Technique, Indirect , Humans , Immunoenzyme Techniques , Intercellular Adhesion Molecule-1/metabolism , Macrophages , Male , Middle Aged , Skin Diseases/metabolism , Vascular Cell Adhesion Molecule-1/metabolism , Xanthomatosis/metabolism , von Willebrand Factor/metabolismABSTRACT
BACKGROUND: Activated mast cells enhance the uptake of mast cell-derived proteoglycan-low-density lipoprotein complexes by macrophages. OBJECTIVE: We sought to investigate mast cell contribution to the pathogenesis of xanthoma. METHODS: Twenty cases of xanthelasma palpebrarum and 6 cases of tuberous xanthoma lesions were analyzed using immunohistochemical staining. RESULTS: Xanthelasma lesions contained up to 5-fold more tryptase-stained mast cells than tuberous xanthoma lesions. Tuberous xanthoma lesions especially showed extensive staining of tryptase around mast cells and within some macrophages and foam cells. More than 99% of mast cells in xanthelasma lesions contained both tryptase and chymase. Approximately 60% of mast cells represented only tryptase in tuberous xanthoma lesions where the ratio of macrophages to tryptase-stained mast cells was extremely high (15:1) as compared with xanthelasma lesions (2:1). LIMITATIONS: A change in mast cell phenotype has not been necessarily proven. CONCLUSION: Mast cells are activated under the microenvironment in which macrophages predominate rather than mast cells, which thus reflects the clinical phenotypes of xanthoma lesions.
