[Normolipemic xanthoma developed on alopecia lesion on a SLE patient--histological study]

A 30-year-old SLE patient developed a xanthoma on her alopecia lesion. Histological examination showed typical lupus changes including immunofluorescence stainings. In addition, there were numerous xanthoma cells existed through the dermis, interlobular spaces of subcutaneous fat tissue, perivascular areas of small blood vessels, and subendothelial spaces and inside of intraluminal thrombosis of subcutaneous small arteries. These xanthoma cells contained granular materials in their cytoplasm. Histochemically, these materials are diastase resistant P.A.S. (+), immunoglobulin (+), Sudan BB (+), Sudan III (+), Nile blue (pinkish red), and yellowish orange autofluorescence suggesting that they are lipofuscin or lipid peroxidation products. Further histological findings showed destruction of sebaceus glands and peri-glandular++ infiltration of lymphocytes and histiocytes. These histiocytes contained phagocytic neutral lipid droplets in their cytoplasm. Very small lipid peroxides were also seen on surface and/or cytoplasm of infiltrating lymphocytes existing not only peri-lobular area but also intraluminal area of blood vessels. The marker profile of these infiltrating lymphocytes are B-cell predominant admixed with some CD8(+) T-cells. These data suggest that the mechanism of developing xanthoma is initiated by immune-complex deposition on basal lamina of sebaceus glands, followed by destruction of sebaceus glands by lympho-histiocytic cells infiltration with some antigen presenting and/or effector cells, and finally xanthoma cells were developed by phagocytosis of lipid peroxides caused by macrophage-derived oxygen radicals. Interestingly, our data suggest that the lipid peroxides, which may act as photosensitizer, may leave the skin and may enter the small vessels carried by lymphocytes. Furthermore the xanthoma cells may also enter the circulation through the small arteries.