1999
DOI: 10.1016/s0190-9622(99)70207-0
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Homocysteinemia and livedoid vasculitis

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Cited by 42 publications
(35 citation statements)
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“…This abnormality has been associated with both venous thrombosis and arterial thrombosis. 36,37 Investigators 38 at our institution compared levels of serum homocysteine in male and female patients who had livedoid vasculopathy with levels in healthy male and female subjects. The mean homocysteine level in female patients with livedoid vasculopathy was higher than in control subjects, which raises the possibility that higher levels of serum homocysteine may be associated with an increased risk of cutaneous or other organ small vessel thrombosis.…”
Section: Commentmentioning
confidence: 99%
“…This abnormality has been associated with both venous thrombosis and arterial thrombosis. 36,37 Investigators 38 at our institution compared levels of serum homocysteine in male and female patients who had livedoid vasculopathy with levels in healthy male and female subjects. The mean homocysteine level in female patients with livedoid vasculopathy was higher than in control subjects, which raises the possibility that higher levels of serum homocysteine may be associated with an increased risk of cutaneous or other organ small vessel thrombosis.…”
Section: Commentmentioning
confidence: 99%
“…There are exceptional reports of cutaneous disease due to hyperhomocysteinemia, and cutaneous changes have rarely been related to hyperhomocysteinemia. It has been reported, in a small series of patients, an association between plasma homocysteine level and livedoid vasculitis, a cutaneous noninflammatory thrombotic vasculopathy involving dermal arterioles (Gibson et al, 1999). Hyperhomocysteinemic patients with CBS deficiency have fine brittle hair and thin skin with hypopigmentation (Carson et al, 1965;Carey et al, 1968;Mudd et al, 1989), which is reversible following treatment that decreases plasma homocysteine (Reish et al, 1995).…”
mentioning
confidence: 99%
“…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.…”
Section: Etiopathogenesismentioning
confidence: 99%
“…21 Among the several reported associations between LV and hypercoagulable states are the following: protein C deficiency, factor V (Leiden) mutation, prothrombin gene mutation, hyperhomocysteinemia, increased levels of lipoprotein(a) and antithrombin deficiency. 8,9,14,20,[30][31][32][33][34][35][36] Consequently, given the heterogeneity of the etiopathogenic factors clinically involved in LV, we propose to classify it according to its etiopathogenesis into primary (idiopathic) or secondary to a known event or condition, with the latter being subdivided into four groups: (i) endothelial damage, (ii) changes in blood flow, (iii) states related to thrombophilias, and (iv) mixed etiopathogenesis.…”
Section: Figurementioning
confidence: 99%