Skin iron deposition characterises lipodermatosclerosis and leg ulcer.

BACKGROUND: It is commonly reported that chronic venous disease (CVD) increases the skin iron content in which the excess is stored as haemosiderin. Despite increasing interest in the role of haemosiderin in venous ulceration, no study has systematically evaluated the occurrence of iron overload in the limbs of patients with CVD. PURPOSE: To evaluate skin haemosiderin deposition in relation to the presence and severity of skin changes in CVD legs designated according to the clinical, etiologic, anatomic and pathophysiologic (CEAP) classification. METHODS: A total of 85 skin biopsies were taken from the medial aspect of 49 limbs with CVD of CEAP clinical stages C2, C3, C4 and C6. The content of ferric ions was assessed by Perl's Prussian Blue (PPB) stain. RESULTS: No haemosiderin deposition was found in normal skin of C2, C3 and C4A legs, in less severe regions of pigmentation and in some parts of more severely affected limbs. Haemosiderin was always present in lipodermatosclerotic skin and ulcers. Occasionally, haemosiderin was found in the apparently normal perilesional skin of C4b and C6 legs. The regenerating dermis at the base of healing ulcers showed none or light haemosiderin deposition. CONCLUSION: 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.

The nature of skin pigmentations in chronic venous insufficiency: a preliminary report.

BACKGROUND: Chronic Venous Insufficiency (CVI) provokes skin pigmentation commonly seen in the gaiter region of the leg. The exact nature and pathogenesis of this are poorly understood. OBJECTIVE: To evaluate the presence of melanin and haemosiderin in histological sections of the skin of limbs with primary varicose veins. METHODS: Histological investigations were performed in 49 biopsies from pigmented and non-pigmented skin of limbs with varicose veins and control limbs. RESULTS: All samples from pigmented skin showed a higher content of melanin than controls. In contrast, haemosiderin was found in only a few biopsies taken from the more severely pigmented skin in areas of lipodermatosclerosis. Erythrocyte diapedesis was observed only where an intense inflammatory process was also present. CONCLUSIONS: 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.