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Xanthomas are plaques or nodules consisting of abnormal lipid deposition and foam cells in skin or in tendons. They do not represent a disease but rather are signs of a variety of lipoprotein disorders. Xanthomas are occasionally seen without an underlying metabolic effect. Xanthomas are thought to develop through several mechanisms. Through scavenger receptors for enhanced low-density lipoprotein (LDL) uptake, macrophages (converted from monocytes) incorporate lipid that has been transported through the capillary walls, thus becoming foam cells. Foam cells can also develop as a result of in situ lipid synthesis by the macrophage. Further, lipid that has been extravasated by the capillaries can also recruit additional foam cells into an already established xanthoma. Extravasated and oxidized LDL recruits foam cells by inducing vascular cellular adhesion molecule and E-selectin.1,2 Local factors such as heat, movement, and friction may increase LDL capillary leakage, and, hence, result in the development of xanthomata.3 These local factors help explain the location of tuberous xanthomas, tendinous xanthomas, and xanthelasmata.
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Clinically, xanthomas can be classified as eruptive, tubo-eruptive or tuberous, tendinous, or planar.4 Planar xanthomas include xanthelasma palpebrarum/xanthelasma, xanthoma striatum palmare, and intertriginous xanthomas. There are characteristic clinical phenotypes associated with specific metabolic defects (Tables 135-1 and 135-2 showing older Frederickson classification).
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