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Skin iron deposition characterises lipodermatosclerosis and leg ulcer
1Department of Anatomy, Sapienza University of Rome, Italy. alberto.caggiati@uniroma1.it
Insights
Chronic venous disease (CVD) leads to skin iron overload, specifically haemosiderin deposition, in severe stages like lipodermatosclerosis and ulcers. This iron accumulation is linked to genetic factors and requires further study in CVD patients.
Area of Science:
- Vascular Medicine
- Dermatology
- Iron Metabolism
Background:
- Chronic venous disease (CVD) is associated with increased skin iron content, stored as haemosiderin.
- The role of haemosiderin in venous ulceration is gaining interest, but systematic evaluation in CVD limbs is lacking.
Purpose of the Study:
- To assess skin haemosiderin deposition in relation to the presence and severity of skin changes in CVD legs.
- Classification of CVD severity was based on the clinical, etiologic, anatomic, and pathophysiologic (CEAP) system.
Main Methods:
- 85 skin biopsies were obtained from 49 limbs with CVD (CEAP stages C2, C3, C4, C6).
- Ferric ion content was quantified using Perl's Prussian Blue (PPB) staining.
Main Results:
- Haemosiderin was absent in normal skin (C2-C4A) and less severe pigmentation.
- Haemosiderin was consistently found in lipodermatosclerotic skin and ulcers.
- Perilesional skin in C4b and C6 stages, and regenerating dermis of healing ulcers, showed variable haemosiderin presence.
Conclusions:
- Iron overload (haemosiderin) is not evident in early CVD skin damage but is consistently present in lipodermatosclerosis and ulcers.
- Severe skin changes in CVD correlate with iron overload, suggesting a potential genetic predisposition.
- Further investigation into disordered iron metabolism in CVD patients is warranted.
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.
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