Cholesterol crystal embolism (CCE) is a systemic refractory disease especially prevalent amongst elderly patients suffering from atherosclerosis. Treatment of this condition remains controversial due to difficulties in diagnosis. Corticosteroid therapy may be an important treatment option despite its elusive mechanisms. To clarify the role of corticosteroid in CCE therapy, we collected the samples from six autopsied subjects with CCE, three of whom were clinically given various doses of corticosteroid to investigate stable atherosclerosis-related substances, advanced glycation end-products (AGE), and several AGE receptors such as scavenger receptor class B type 1 (SR-B1), receptor for AGE (RAGE), and galectin-3 in the liver tissues and atherosclerotic areas by immunostaining using a tissue macro-array technique. An intense expression of AGE and its receptors was identified in the enlarged Kupffer cells of CCE cases, which were given relatively high doses of corticosteroid. In addition, numerous mononuclear cells in the intimal atheromatous plaque presented strong expressions of AGE and SR-B1. In conclusion, we speculated that corticosteroid treatment for CCE may upregulate the activations, including phagocytic capacity of Kupffer cells mediated by overexpression of RAGE and scavenger receptors, resulting in efficient clearance of the lipid substances from the blood circulation released from atherosclerotic areas.