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Failure of Low-Dose Methotrexate in the Treatment of Scleredema diabeticorum in Seven Cases

299 whereas skin of the extremities, the least frequent site of BCC development, was found to express signifi cantly more MCs (33.8 8 1.4 MCs/mm 2 ) than trunkal skin (p ! 0.001), indicating that skin site MC numbers do not correlate with BCC incidence. In contrast, skin MC numbers in the three distinct anatomical areas investigated correlated well with BCC growth patterns, i.e. large skin MC populations were found to be associated with a high prevalence of nodular BCCs, the most proliferating and most common BCC subform ( table 1 ). At head skin sites, nodular BCC was found to be by far the predominant BCC type (86%), whereas trunkal skin sites exhibited the lowest percentage of nodular BCCs (12%, table 1 ). Skin of the extremities (intermediate MC numbers) exhibited an intermediate percentage of nodular BCC (20%, table 1 ). Our fi ndings suggest that local skin MC populations promote the growth, but not the onset of BCCs and, thus, confi rm and extend recent fi ndings by Grimbaldeston et al. [8, 9] , who show that numbers of MCs at sun-exposed skin sites, i.e. skin sites with high MC numbers, do not correlate with an increased risk to develop BCC at these sites. On the other hand, high overall numbers of dermal MCs, as assessed by counting MCs at sun-protected skin sites, were found to predispose to BCC development [9] . The latter role of dermal MCs, as confi rmed by this report, does not critically involve local MC populations and most likely results from systemic immunosuppression induced by activated skin MCs, e.g. after UVB exposure [8, 9] . Thus, skin MCs may facilitate BCC development by two independent mechanisms: (1) widespread skin MC activation (and the resulting immunosuppression) could increase the host’s general susceptibility to develop BCC; (2) subsequently, local MC populations may promote increased, i.e. nodular, tumor growth, at sites of BCC development. Notably, our fi ndings cannot explain why large local MC populations predispose to nodular BCC growth. Several possible mechanisms, including direct effects of MCs and MC products on keratinocyte proliferation and tumor vascularization, are currently under investigation as is the possible role of dermal MCs in other hyperproliferative skin disorders.