Large molecular weight sodium dextran sulfate (SDS) injection into the dermis of both normolipemic rabbits and hypercholesterolemic rabbits induced infiltration of histiocytes and foam cells. Sudan III staining showed that the histiocytes and foam cells of hypercholesterolemic rabbits accumulated lipids similarly to xanthoma foam cells. The accumulated lipids increased as the injection was repeated at the same site. However, the lipid accumulation was minimal in the histiocytes of normolipemic rabbits. As determined by quantitative analysis of lipid composition in the lesions of hypercholesterolemic rabbits, cholesterol esters remarkably increased concomitantly with injection frequency. Free cholesterol accumulation was less pronounced than cholesterol ester. In normolipemic rabbit dermis, accumulation of free cholesterol was insignificant and cholesterol esters did not accumulate progressively with repeated SDS injections. Apparently the foam cells of hypercholesterolemic rabbits actively incorporated serum low density lipoproteins (LDL) and cholesterol was esterified in the foam cells. On the other hand, LDL were minimally incorporated into histiocytes in the normolipemic state. The intradermal SDS injection is a beneficial experimental model for further investigations on the mechanisms of lipid accumulation and the intracytoplasmic lipid metabolism of xanthoma foam cells.

Xanthoma was produced in diet-induced hypercholesterolemic rabbits by intradermal dextran sulfate injections. The serum cholesterol level returned to the normal range at about 10 weeks after ending the cholesterol diet. Gross observations after cessation of the cholesterol diet revealed a decrease in xanthomatous infiltrations. However, the dense foam cell infiltrations and cholesterol accumulations showed no signs of regression at even 9 months after ending the cholesterol diet. Signs of foam cell migration into the blood stream were not observed. The persistence of the xanthoma may be due to a lack of acceptors, such as high-density lipoproteins, that remove the cholesterol from the foam cells. During our 9-month observation period, some foam cells were degenerated and a few were fused with each other to transform into Touton-type giant cells. Nonfoamy histiocytes were infiltrated around these degenerating foam cells. The histiocytes may have transformed into foam cells by incorporating the lipids of the degenerated foam cells.

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Granuloma annulare is a degenerative disease of the skin histopathologically characterized by focal degeneration of collagen with a surrounding infiltrate of lymphoid cells, histiocytic cells, and multinucleated giant cells. Immunological abnormalities such as delayed-type hypersensitivity and vasculitic origin are suspected in the pathogenesis. We describe three patients with generalized granuloma annulare, in whom autoantibodies, including antinuclear antibody, antithyroid stimulating hormone receptor antibody, and immune complex, were detected.

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