The frequent occurrence of normal SVs in varicose limbs of all patients does not support the crucial role commonly credited to SVs in the pathogenesis of primary varicosities. Moreover, the SV trunks were normal in most varicose limbs from young patients. These findings suggest that varicose disease may progressively extend in an antegrade fashion, spreading from the STVs to the SVs. This hypothesis suggests that the saphenous trunks could be spared in the treatment of a relevant number of varicose legs. Prospective longitudinal studies with serial duplex evaluations of large series of extremities are necessary to confirm this hypothesis.
Iron overload is not present in the less severe stages of skin damage due to CVD but lipodermatosclerosis and leg ulcers are always accompanied by haemosiderin deposition. In fact, no severe skin changes occur in CVD legs until iron overload occurs. Our results are in agreement with previous reports suggesting that a genetic inability to counteract skin iron overload is present in these patients. A more detailed analysis of disordered iron metabolism should be undertaken in CVD patients.
Our findings suggest that in the initial phases of skin changes due to venous disease, pigmentation is attributable to melanin. Haemosiderin seems to play a role in the evolution of skin changes toward lipodermatosclerosis and ulceration. Erythrocyte diapedesis is likely to occur only during acute phases of the inflammatory process. Further investigations are needed to explain the cause and the exact cellular and molecular mechanisms responsible for hypermelanisation occurring in early phases of skin changes in CVI.
Our findings confirm the occurrence of ED during CVD. However, it was found only in concomitance of severe dermal inflammation. Hemosiderin deposition in the absence of actual ED could be explained with previous healed episodes of skin inflammation. However, ED is not likely the only cause of skin iron overload, which could also occur by a molecular mechanism. Further studies are needed to define the mechanism of iron deposition in the skin of legs afflicted with CVD.
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