Atrophie blanche

Vasculopatia livedoide: uma doença cutânea intrigante

“…17 However, we disagree with this point of view due to the large differential diagnosis involved in the disease as well as to the fact that biopsy only caused difficult-to-heal ulcers among our patients on few occasions. 8,9,58 The initial challenge in the histopathological diagnosis of LV is to obtain an adequate skin sample, which represents from the epidermis to the dermo- 4: System of coagulation, natural anticoagulation and fibrinolysis.…”

“…9,[12][13][14][15][16] Changes in the blood flow not only include venous insufficiency, but also diseases that lead to hyperviscosity syndrome such as chronic myelogenous leukemia, cryoglobulinemia and heavy chain disease. 9,17 Hypercoagulable states are rare situations and still partially unknown. They are currently classified as hereditary -which include genetic defects of the coagulation cascade and of fibrinolysis -and acquired.…”

“…34 There is deposition of fibrin on the vessel walls in the initial stages, and deposition of immunoglobulins and complement is detected in later stages. 1,58,63,64 17,34 Some authors have interpreted the frequent finding of IgM in DIF studies on LV as a consequence of the sequestration of large complexes of immunoglobulin M, which has very high molecular weight, by deposits of fibrin in damaged vessels. 65 Therefore, the histopathological findings in LV allow us to better classify it as vasculopathy instead of immune-complex-mediated necrotizing vasculitis due to: (i) absence of neutrophilic polymorphonuclear leukocytes and nuclear fragmentation in the area around dermal vessels early in the process; (ii) no permeation of the vessel wall by leukocytes; (iii) fibrin deposition and hyalinization of the vessel wall; (iv) normal serum levels of the complement in most patients and absence of detectable circulating immune complexes.…”

“…It is present in other conditions such as SLE, scleroderma, Degos disease and more frequently in chronic venous insufficiency (9% to 38% of the patients), with or without ulceration, thus simply representing scar morphology resulting from various types of injury and not indicative of a nosological entity. 17 Once the required differential diagnoses have been carried out and the presence of LV is confirmed, an accurate laboratory evaluation aimed at determining the presence of abnormalities suggestive of autoimmune connective tissue diseases, congenital and acquired thrombophilias, paraproteinemia, serology for hepatitis B and C and HIV test must be performed. Particular attention should be given to the quality of the skin biopsy, since LV is defined based on clinical and histopathological findings.…”

“…42 Several therapeutic approaches have been employed with varying degrees of success. 17 The use of topical, systemic and intralesional corticosteroids has shown little or no efficacy. 17 However, all forms of treatment proposed for LV are based on reports of isolated cases or case series.…”