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[Clinicopathological and immunohistochemical studies of xanthogranulomatous cholecystitis--possible pathogenetic role of cell mediated immunity].

Clinicopathological and immunohistochemical studies were performed on 22 cases of xanthogranulomatous cholecystitis (XGC). Incidence of XGC was 3.6% of surgically resected gallbladder diseases. All cases of XGC were associated with cholelithiasis in which cholesterol gallstones were 6 times as many as pigment ones. XGC was frequently accompanied by incarceration of gallstones. In cholecystography, two-thirds of gallbladders were not visualized. Histologically, the granulomatous lesion of XGC consisted of accumulations of foam cells, lymphocytes, variable numbers of giant cells, granulocytes and fibroblastic cells. Although there had been no established theory in relation to the origin of foam cells, it is considered that foam cells were derived from monocyte/macrophages because they reacted variably with lysozyme, alpha 1-antichymotrypsin and alpha 1-antitrypsin, and almost invariably with OKM 1 and EBM 11 antibodies. Interspersed among macrophage foam cells, many T lymphocytes were identified. In terms of T cell subsets, CD 8 positive lymphocytes outnumbered CD 4 positive lymphocytes. Electron microscopy demonstrated intimate apposition of T lymphocytes to macrophages or macrophage foam cells. HLA-DR was expressed by most macrophages, macrophage foam cells and T lymphocytes. In conclusion, the results suggest that the features of XGC are those of granulomatous inflammation characterized by accumulation of macrophages, macrophage derived foam cells and activated T cells. It is suggested that delayed type hypersensitivity reaction of cell mediated immunity is operative in the pathogenesis of XGC.