Mastocytosis is characterized by the abnormal growth and accumulation of neoplastic mast cells in one or more organs. The skin is the most common site for the abnormal accumulation of mast cells, known as cutaneous mastocytosis. Clinical categories of cutaneous mastocytosis, in order of frequency of occurrence, include urticaria pigmentosa, mastocytoma, diffuse cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans (TMEP). It has been reported that mastocytoma had developed in a patient in association with another form of cutaneous mastocytosis. Okun and Bhawan reported a combined melanocytoma-mastocytoma in a patient of nodular mastocytosis, and Wood et al. reported a case of fibrous mastocytoma in a patient with generalized cutaneous mastocytosis. Our patient had had urticaria pigmentosa since childhood and two years prior to examination, combined mastocytoma-hemangioma had developed as another histopathologic features from those previously reported.
The pathogenesis of developing combined masto- cytoma-hemangioma is not clear, but there is some evidence that some mast cell mediators could induce neovascularization. Increased numbers of mast cells are often associated with rapidly growing capillaries in some conditions such as chronic inflammation or tumors. An increased number of mast cells was found in the growing stages of strawberry hemangioma, and a significantly greater number of mast cells was found in angiolipomas than in classic lipomas. These examples lead us to suggest that mast cells might be associated with the growth of new vessels. It has been reported that some mast cell mediators might contribute to various aspects of neovascularization. Taylor and Folkman showed that heparin could enhance angiogenesis induced by tumor extracts implanted in a chick embryo. It was revealed that heparin induced angiogenesis by significant migration of endothelial cells. Heparin has also been found to have a very high binding affinity for endothelial cell growth factors, some of which are angiogenic. Moreover, Qu et al. suggested that mast cells may be a significant source of tissue bFGF, one of the most potent angiogenic factors has been shown to induce angiogenesis, in angiogenic condition. Using specific antibodies, they demonstrated a marked spatial correlation between bFGF immunoreactivity and mast cells in cutaneous hemangioma. Such correlation indicates that mast cells could be a source of tissue bFGF during neovascularization. Boesiger et al. reported that human mast cells can produce and secrete VPFs and VEGFs, which are important regulators of neovascularization. It was revealed that mast cells can secrete VPF and VEGF upon activation via the Fc £ receptor (Fc £ RI). Moreover, they found that the IgE-dependent secretion of VPF and VEGF can be significantly increased in mast cells, which undergo IgE-de- pendent upregulation of their surface expression of Fc £ RI. In particular, they found that neoplastic mast cell lines can secrete greater amounts of VPF and VEGF than nonneoplastic mast cells. According to these findings, we suggest that the development of hemangioma could be induced by mast cell mediators such as heparin, basic fibroblast growth factor, vascular permeability factor, and vascular endothelial growth factor, which have angiogenic properties.
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