1986
DOI: 10.1001/archderm.122.8.855
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Idiopathic atrophie blanche: treatment with low-dose heparin

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Cited by 9 publications
(12 citation statements)
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“…A similar fibrin occlusive vasculopathy is seen in biopsies of leg ulcers due to livedoid vasculopathy. Livedoid vasculopathy is associated with impaired fibrinolysis from a variety of genetic and acquired causes [57] and heparin an anticoagulant with profibrinolytic actions has been effective in some cases [810]. We postulate that dysregulation of the complement and coagulation cascades with inadequate fibrinolysis and angiogenesis may contribute to delayed healing in scleroderma- associated lower extremity ulcers.…”
Section: Introductionmentioning
confidence: 99%
“…A similar fibrin occlusive vasculopathy is seen in biopsies of leg ulcers due to livedoid vasculopathy. Livedoid vasculopathy is associated with impaired fibrinolysis from a variety of genetic and acquired causes [57] and heparin an anticoagulant with profibrinolytic actions has been effective in some cases [810]. We postulate that dysregulation of the complement and coagulation cascades with inadequate fibrinolysis and angiogenesis may contribute to delayed healing in scleroderma- associated lower extremity ulcers.…”
Section: Introductionmentioning
confidence: 99%
“…The deposition of fibrinoid material in dermal vessels with secondary ischemic change of the overlying skin, elevated serum fibrinopeptide A levels, 12 high incidence of antiphospholipid antibodies, defective release of tissue plasminogen activator, 13 and increased levels of plasminogen activator inhibitor in plasma 8 from patients with livedoid vasculitis support an underlying thrombo‐occlusive process. Clinical improvement obtained using fibrinolytics, 3 pentoxifylline, 5 anticoagulant, 6 and antithrombotic therapy also favors this pathogenetic mechanism. Specific histologic findings, such as thickened blood vessel walls, occasional deposition of immunoreactants and fibrin, and the possible association with immune‐mediated diseases, suggest a potential pathogenetic role of immunologic mechanisms 14,15 .…”
Section: Discussionmentioning
confidence: 99%
“…The current therapeutic approach to livedoid vasculitis is to use drugs that stimulate endogenous fibrinolytic activity, inhibit thrombus formation, or cause vasodilatation. Aspirin and dipyridamole, nicotinic acid, low‐dose heparin or warfarin, 6 dextran, 4 and pentoxifylline 5 have been used. Intravenous infusions of tissue plasminogen activator, which lyzes microvascular thrombi, restores circulation, and promotes wound healing, have been successfully used 8 .…”
Section: Discussionmentioning
confidence: 99%
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“…Since impaired hemostasis and fibrinolysis play an important role in the etiology, therapy should modulate or interfere with microcirculatory disturbances. Three major groups of drugs are used in the treatment of AB: 1) drugs that stimulate endogenous fibrinolytic activity (combination of phenformin and ethylestrenol, tissue plasminogen activator, aspirin, and/or warfarin) 4, 7 ; 2) drugs that inhibit thrombus formation (antiplatelet and anticoagulant drugs: aspirin, dipyridamole, prostaglandin E 1 , pentoxifylline, heparin) 8–10 ; and 3) vaso‐dilating drugs (nifedipine, sulfasalazine) 1, 3 …”
Section: Classification Of Atrophie Blanchementioning
confidence: 99%