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Abstract

Tsiridis et al. presented an unusual case of avascular necrosis in the peripheral bone, which was later found to be combined with a glioblastoma in the brain. They suspected the avascular necrosis was caused by an endogenous inhibitor of angiogenesis, such as endostatin or transforming growth factor β, secreted from the glioblastoma tissue. Their hypothesis is very attractive. However, it is necessary to show data supporting a direct causal relationship between a glioblastoma and avascular necrosis of the peripheral bone. Detection of the tissue levels or serum levels of endostatin or transforming growth factor β could support the hypothesis. Although we showed increased levels of tissue endostatin in glioblastomas (1), we unfortunately did not examine the levels of endostatin in the serum for these patients. Furthermore, there have been no reports in which glioblastomas or other tumors secreting high levels of endostatin are combined with avascular necrosis of the peripheral bone (2, 3). With regard to the systemic effects of antiangiogenic therapies suggested by Tsiridis et al., no side effects such as avascular necrosis of the peripheral bone have been reported in a Phase I clinical trial of recombinant endostatin (4). However, this case report by Tsiridis et al. will promote further careful survey for the systemic effects of antiangiogenic factors in tumors secreting high levels of endostatin as well as in clinical application of recombinant endostatin.