1975
DOI: 10.1001/archderm.111.2.188
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Livedo vasculitis (the vasculitis of atrophie blanche). Immunohistopathologic study

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Cited by 37 publications
(26 citation statements)
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“…Previous studies have described characteristic thick, intense staining of vessel walls corresponding to hyalinized vessels on hematoxylin-eosin-stained sections. 48 The deposition of these factors, especially fibrin, may be potentially explained by a prothrombic and fibrinolytic state, as has been supported by the finding of elevated fibrinopeptide levels in patients with livedoid vasculopathy. 8 Complement deposition may be a consequence of activation of the coagulation pathway.…”
Section: Commentmentioning
confidence: 90%
“…Previous studies have described characteristic thick, intense staining of vessel walls corresponding to hyalinized vessels on hematoxylin-eosin-stained sections. 48 The deposition of these factors, especially fibrin, may be potentially explained by a prothrombic and fibrinolytic state, as has been supported by the finding of elevated fibrinopeptide levels in patients with livedoid vasculopathy. 8 Complement deposition may be a consequence of activation of the coagulation pathway.…”
Section: Commentmentioning
confidence: 90%
“…3 The underlying cause is not yet fully understood; however, the disease has been reported in individuals with altered coagulation, including factor V Leiden mutation, 4 protein C deficiency, 5 antiphospholipid antibody syndrome, 6 increased plasma homocysteine levels, 7 abnormalities in fibrinolysis, 8 and increased platelet activation. 9 Because potential thrombogenic mechanisms may be involved in the disease pathogenesis, 10,11 anticoagulant therapy is often tried.…”
Section: Commentmentioning
confidence: 99%
“…We did not detect any significant sign of leukocytoclastic vasculitis. Although various reports have revealed the deposition of immunoreactants in blood vessels of patients with LV, 9 the "vasculitic" pathogenesis of this disease has never been sufficiently supported. Numerous investigators consider LV an occlusive vasculopathy.…”
Section: Commentmentioning
confidence: 99%
“…5 On the basis of the clinical evolution, the improvement during fibrinolytic and anti- platelet therapy, [6][7][8] and the detection of elevated serum fibrinopeptide A levels, 2 LV is thought to be mediated by a vasocclusive mechanism. Nevertheless, specific histological findings, such as thickened blood vessel walls, occasional deposition of immunoreactants, and fibrin, 9 and the possible association with immune-mediated diseases suggest a potential pathogenetic role of immunological mechanisms. Tissue plasminogen activator treatment was recently reported to be effective in LV.…”
Section: Main Outcome Measuresmentioning
confidence: 99%