Livedo vasculitis with protein C system deficiency

Baccard, M.

doi:10.1001/archderm.128.10.1410

Cited by 15 publications

(24 citation statements)

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“…It can be associated with systemic disorders like SLE or present in an "ideopathic" form [60]. A number of studies report about different coagulation abnormalities: elevated fibrinopeptid A [62], defective release of vascular plasminogen activator [73], decreased thrombomodulin expression [100] and protein C deficiency [4].Acland et al have suggested that livedoid vasculopathy may be a manifestation of antiphospholipid syndrome [1].…”

Section: ■ Livedoid Vasculopathymentioning

confidence: 99%

The spectrum of differential diagnosis in neurological patients with livedo reticularis and livedo racemosa

2005

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Livedo is a cutaneous sign of striking violaceous netlike patterned erythema of the skin. This dermatological phenomenon is of special interest in the differential diagnosis in neurological patients. In 1907 Ehrmann distinguished two different patterns of livedo: the pathological livedo racemosa and the physiological livedo reticularis. Despite important clinical differences, in the English language literature the heading livedo reticularis is still used for all types of livedo. A literature review about the spectrum of differential diagnosis in patients with livedo reticularis (especially cutis marmorata and amantadine-induced livedo reticularis) and livedo racemosa (especially Sneddon's syndrome, Divry-van Bogaert syndrome, systemic lupus erythematosus, antiphospholipid antibody syndrome, polyarteritis nodosa, cholesterol embolization syndrome, livedoid vasculopathy and haematological diseases) is provided.

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Section: ■ Livedoid Vasculopathymentioning

confidence: 99%

The spectrum of differential diagnosis in neurological patients with livedo reticularis and livedo racemosa

2005

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“…1,2 Patients with LV exhibit various coagulation abnormalities, including cryoglobulinemia, protein C deficiency, antithrombin III deficiency, factor V Leiden mutation, and hyperhomocysteinemia. [3][4][5] Current treatment strategies focus on anticoagulant, antiplatelet, and fibrinolytic therapies, but these treatments usually produce slow responses and unsatisfactory results. Impaired endothelial cell function can induce vessel inflammation and influence coagulation and fibrinolysis, resulting in atherosclerotic and several vascular thrombotic diseases.…”

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confidence: 99%

Association between peripheral vascular endothelial dysfunction and livedoid vasculopathy

Yang

Shen

Hui

et al. 2012

Journal of the American Academy of Dermatology

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“…These data indicated that venous thrombosis occurred only in a minority of all protein C-deficient families, suggesting that other as yet undefined factors such as a second thrombotic defect are likely to modulate the phenotypic expression of heterozygous protein C deficiency. 2 In 1992, Baccard et al 3 reported a case of livedoid vasculopathy (under the designation livedo vasculitis) associated with protein C deficiency and hypothesized that protein C deficiency might be a potential pathogenetic factor causing a thrombotic origin of livedo vasculopathy. Although the authors pointed to the possibility of coincidence of these two conditions, our further case supports a possible relationship between these two disorders, suggesting that protein C deficiency may be one cause of the hypercoagulable state in patients with livedoid vasculopathy.…”

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confidence: 99%

Livedoid vasculopathy associated with heterozygous protein C deficiency

Boyvat

̧i

Babikir

et al. 2000

British Journal of Dermatology

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Livedoid vasculopathy is characterized by recurrent painful ulceration of the feet, ankles and legs that heals with residual white atrophic scars. For many years, livedoid vasculopathy has been considered to be a primary vasculitic process. Recently, however, there has been a trend towards considering livedoid vasculopathy as an occlusive vasculopathy due to a hypercoagulable state. Livedoid vasculopathy (under the designation livedo vasculitis) was first reported to be associated with protein C deficiency in 1992. We describe an additional patient with livedoid vasculopathy associated with heterozygous protein C deficiency. This second reported case suggests that protein C deficiency may be one cause of the hypercoagulable condition in these patients and demonstrates the necessity for further investigation of thrombogenic factors underlying the disease.

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Livedo vasculitis with protein C system deficiency

Cited by 15 publications

References 0 publications

The spectrum of differential diagnosis in neurological patients with livedo reticularis and livedo racemosa

The spectrum of differential diagnosis in neurological patients with livedo reticularis and livedo racemosa

Association between peripheral vascular endothelial dysfunction and livedoid vasculopathy

Livedoid vasculopathy associated with heterozygous protein C deficiency

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