Pentoxifylline (Trental) Therapy for the Vasculitis of Atrophie Blanche

Sauer, Gordon C.

doi:10.1001/archderm.1986.01660160030012

Cited by 44 publications

(11 citation statements)

References 3 publications

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“…These studies suggest that the thrombosis found to occur in livedoid vasculitis is part of a primary pathophysiological mechanism. In addition, a number of patients with livedoid vasculitis have responded to antithrombotic and antifibrinolytic agents including heparin,19 tPA,11, 21 pentoxyphylline,8, 9, 33, 34 aspirin and dipyridamole,8, 20 long‐term anticoagulants,6, 12 danazol,17, 38 ketanserin,32 beraprost,37 and prostacyclin 16. A single report of intravenous immunoglobulin in livedoid vasculitis suggested a possible response 33.…”

Section: Discussionmentioning

confidence: 99%

Mononeuropathy multiplex in association with livedoid vasculitis

et al. 2003

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Livedoid vasculitis is a chronic dermatological disorder associated with petechiae and recurrent, unusually shaped ulcers that heal to form hyperpigmentated areas and atrophie blanche. This condition is more correctly termed a vasculopathy, rather than a vascultis, and is often associated with an underlying hypercoagulable disorder. We report a patient with livedoid vasculitis and mononeuropathy multiplex. We propose that peripheral nervous system involvement arises from multifocal areas of ischemia due to fibrin and thrombin deposition within both the wall and lumen of vasa nervorum.

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Section: Discussionmentioning

confidence: 99%

Mononeuropathy multiplex in association with livedoid vasculitis

et al. 2003

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“…92–93 It improves membrane flexibility of erythrocytes, reduces platelet aggregation, and decreases vessel fibrinogen concentration by increasing fibrinolytic activity. 79 Although it is indicated mainly for intermittent claudication, it has been useful in the treatment of ischemic ulcers, 94 livedoid vasculitis, 95 stasis ulcers, 94 sickle cell ulcers, 79 necrobiosis lipoidica diabeticorum, 96 and Raynaud's phenomenon. 97 It is noted to have a mild vasodilatory effect.…”

Section: Vascular Drugsmentioning

confidence: 99%

The effects of drugs on wound healing–‐part II. Specific classes of drugs and their effect on healing wounds

et al. 2000

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Classes of drugs in wound healingDrugs can inhibit or assist wound healing. The effect of a speci®c drug depends on its mechanism of action, dosage, route, and administration in relation to the speci®c phase of wound healing. A discussion of the major classes of drugs that impact wound healing follows, with Tables 1±8 summarizing the effects of major classes of drugs. Generic and trade names used in this paper are summarized in Table 9. Table 1 lists the effects of anti-in¯ammatory agents on wound healing. Anti-in¯ammatory agents CorticosteroidsCorticosteroids affect almost every phase of wound healing because of their inhibitory effect on gene expression in various cells. The in¯ammatory phase of wound healing is affected as corticosteroids inhibit prostaglandin synthesis. 1±4 The recruitment and phagocytic properties of neutrophils 5 and macrophages 6 are decreased causing delayed removal of bacteria and foreign bodies. 7 Lymphocyte recruitment and antibody formation by B lymphocytes is reduced. 2 The antimitotic activity 8 causes decreased epithelial regeneration 4 and granulation tissue formation 4,9 affecting the tissue formation phase. A thinned epidermis occurs due to a reduced rate of keratinocyte proliferation and an increased rate of differentiation. 9,10 Granulation tissue formation is reduced due to decreased ®broblast proliferation, 9 resulting in less collagen, 11 proteoglycans, and glycosaminoglycans. 12±14 A decreased oxygen and reduced nutrient supply 14 may result from steroid-induced vasoconstriction caused by the inhibition of the potent vasodilator prostaglandin E 2 (PGE 2 ) 15 and by the enhanced smooth muscle contraction of vessel walls. 14 As the number of macrophages in the tissue is decreased under the in¯uence of steroids, cytokine stimulation provided by macrophages for normal ®broplasia and angiogenesis is diminished. 6 The tissue remodeling phase is affected by decreased collagen and ground substance synthesis. Decreased numbers of ®broblasts are seen and wound contraction is reduced. 16 Steroid atrophy leads to a thinned dermis and the development of striae 17 (Fig. 1). Interestingly, corticosteroids also decrease collagen degradation by decreasing collagenase production. 18 The most pronounced effects are noted when steroids are administered during the early in¯ammatory phase. 19±21 The suppression of macrophage-orchestrated events by steroids in early in¯ammation is thought to play a role. 22 While oral doses of prednisone (above 10 mg per day) adversely affect wound healing during the ®rst 3 days, high-dose prednisone (at or above 40 mg per day) is needed to effect ®broplasia and collagen remodeling during subsequent days. 21 Inhibition of wound contracture in open wounds occurs regardless of the timing of corticosteroid administration. 20 Steroids affect cells by altering gene expression after they cross cell membranes, bind to cytoplasmic receptors, and translocate into the nucleus. 23,24 The degree of inhibition of gene expression is related to the potency of the steroid. 2...

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“…118 , 119 Pentoxifylline has been used because of its improving effect on erythrocyte deformability and lowering effect on blood viscosity. 120 , 121 Both aspirin and pentoxifylline have, besides the above‐mentioned properties, a positive effect on rheology and prevent sludge formation. Anticoagulants were first suggested in 1962.…”

Section: Therapymentioning

confidence: 99%