Abstract
BCNU wafer (BW) is known to increase risk of edema, frequently accompanied by enhancing lesions. The underlying mechanism is not clarified. We performed close histological examination including electron microscopy of the mass-effect-causing enhancing lesion resected from 4 patients (3 glioblastomas and 1 anaplastic oligodendroglioma) 2-33 months after the BW implantation. There noticed were two types of tissue damage in the resected lesions: 1) necrosis in immediate contact with the wafer or its remnant, and 2) necrosis with marked vasculopathy affecting arterial branches and venules. The former contained phagocyted or non-phagocyted crystalline structured polymer, and translucent spherical bodies with calcified core that were not surrounded by viable cells. In the latter, marked degeneration of arterioles were observed, suggesting relatively prolonged exposure to toxic substances such as the released BCNU, degraded polymer and cytokines. Similar type of vasculopathy had been observed in monkey brains implanted with the BCNU-free polymer. Our data suggest that the edema and neecrotic response induced by the BW implantation are results of not only the direct effect of the released drug, but also of inflammatory vasculopathy caused by the degraded polymer itself that occur even in later phase.
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