Difficult Management of Livedoid Vasculopathy

Françès, Camille; Barète, Stéphane

doi:10.1001/archderm.140.8.1011

Cited by 38 publications

(29 citation statements)

References 3 publications

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“…The disease affects primarily the small blood vessels in the lower extremities and is typified by persistent livedo reticularis associated with recurrent painful ulcerations that heal with white atrophic scars [1,2]. The pathogenesis of LV remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…The skin lesions usually affect the small blood vessels in the lower extremities and are recognizable by focal purpura, depigmentation and shallow ulcers that heal with white atrophic scars [1]. While no definitive treatment exists for LV, smoking cessation, anti-platelet therapy, immunosuppressive treatment, and anabolic steroids are often included in the therapeutic ladder [2]. Thrombophilic conditions also occur frequently in patients with LV [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

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Enhanced functional stability of plasminogen activator inhibitor-1 in patients with livedoid vasculopathy

Ağırbaşlı

Eren

et al. 2011

J Thromb Thrombolysis

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Livedoid vasculopathy (LV) is a chronic, recurrent, painful cutaneous disease with distinctive clinical features and an uncertain etiology. The skin lesions are recognizable by focal purpura, depigmentation and shallow ulcers. Thrombophilic conditions occur frequently in patients with LV. While no definitive treatment exists for LV, smoking cessation, antiplatelet therapy, immunosuppressive treatment, and anabolic steroids are often included in the therapeutic ladder. Recently, a possible link between LV and impaired fibrinolysis was established as cutaneous LV lesions responded to tissue plasminogen activator (t-PA) infusion suggesting that inhibition of the fibrinolysis through plasminogen activator inhibitor-1 (PAI-1) activity may determine the disease course in patients with LV. In this study, we investigated PAI-1 antigen (Ag) and activity levels in 20 patients with biopsy proven LV (mean age 26 ± 11, M/F = 7/13, median disease duration 3.5 years). All patients received antiplatelet treatment with aspirin and/or dipyrimadole and 14 patients received anabolic steroids or immunosuppressive treatment. Fasting PAI-1 Ag and activity levels were measured at 9 AM in all patients. Both Ag (34 (26) ng/ml) (median (interquartile range)) and specific activity (17 (23) IU/fmole) levels of PAI-1 were moderately elevated in LV patients compared to the controls, however, PAI-1 kinetic studies demonstrated markedly enhanced stability of PAI-1 activity in plasma from patients with LV. Specific activity at 16 h was significantly higher than expected specific activity levels (7 (11) vs. 0.07 (0.09) IU/fmole, P < 0.01). While the exact mechanism of increased stability of PAI-1 activity is not known, it may be due to post-translational modifications or increased binding affinity for a stabilizing cofactor. In conclusion, enhanced stability of PAI-1 may contribute to the pathophysiology of LV, and systemic or local treatment with PAI-1 inhibitors may offer a potential treatment alternative in patients with LV.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Enhanced functional stability of plasminogen activator inhibitor-1 in patients with livedoid vasculopathy

Ağırbaşlı

Eren

et al. 2011

J Thromb Thrombolysis

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“…Although long-term warfarin therapy after the administration of tissue plasminogen activator has been reported in the literature as a successful treatment for livedoid vasculopathy, Francès and Barete 27 recently discussed the efficacy of the use of vitamin K antagonists alone, specifically fluindione, in the treatment of refractory livedoid vasculopathy. 21 The use of vitamin K antagonists in the treatment of this disorder is a logical choice because of the reported success of other antico- agulant medications, such as heparin.…”

Section: Commentmentioning

confidence: 99%

Warfarin Therapy for Livedoid Vasculopathy Associated With Cryofibrinogenemia and Hyperhomocysteinemia

Browning¹,

Callen²

2006

Arch Dermatol

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“…8 Several authors have used mini-doses of heparin or even full dose anticoagulation. 8,[19][20][21]32,43,45,48,67,[92][93][94][95] Both unfractionated heparin (UFH) and low molecular weight heparins (LMWHs) have established employment in the prevention and treatment of venous thromboembolism (VTE) and as adjunctive therapy in atheroembolic syndromes. 96 LMWHs are replacing UFH in anticoagulation therapy due to a number of advantages, which include a more predictable pharmacokinetic profile and ease of use.…”

Section: (Vi) Therapies Of Still Poorly Understood Mechanismsmentioning

confidence: 99%

Vasculopatia livedoide: uma doença cutânea intrigante

Criado

Rivitti

Sotto

et al. 2011

An. Bras. Dermatol.

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Livedoid vasculopathy is a skin disease that occludes the blood vessels of the dermis. It has a pauciinflammatory or non-inflammatory nature. It is characterized by the presence of macular or papular, erythematous-purpuric lesions affecting the legs, especially the ankles and feet, and producing intensely painful ulcerations, which cause white atrophic scars called "atrophie blanche". This review includes studies and case reports found in the medical literature regarding the etiopathogenic associations of the disease, particularly those related to thrombophilia, their histopathological findings and the therapeutic approaches used in the difficult clinical management of these cases. Keywords: Leg ulcer; Livedo reticularis; Thrombophilia; Thrombosis; Venous thrombosis Resumo: A vasculopatia livedoide é uma afecção cutânea oclusiva dos vasos sanguíneos da derme, de caráter pauci-inflamatório ou não-inflamatório. Caracteriza-se pela presença de lesões maculosas ou papulosas, eritêmato-purpúricas, nas pernas, especialmente nos tornozelos e pés, as quais produzem ulcerações intensamente dolorosas, que originam cicatrizes atróficas esbranquiçadas, denominadas "atrofia branca". Nesta revisão, abordamos os estudos e relatos de caso da literatura médica referentes às associações etiopatogênicas da doença, particularmente as que se referem aos estados de trombofilia, seus achados histopatológicos e abordagens terapêuticas empregadas na difícil condução clínica destes casos.

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Difficult Management of Livedoid Vasculopathy

Cited by 38 publications

References 3 publications

Enhanced functional stability of plasminogen activator inhibitor-1 in patients with livedoid vasculopathy

Enhanced functional stability of plasminogen activator inhibitor-1 in patients with livedoid vasculopathy

Warfarin Therapy for Livedoid Vasculopathy Associated With Cryofibrinogenemia and Hyperhomocysteinemia

Vasculopatia livedoide: uma doença cutânea intrigante

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