Disease relevance of Leg Ulcer

• We treated chronic vasculitic leg ulcers in rheumatoid arthritis and systemic sclerosis by topical application of nerve growth factor (NGF) [1].
• Pseudomonas aeruginosa exotoxin A antibodies in rapidly deteriorating chronic leg ulcers [2].
• Recurrent bilateral leg ulcers developed in two patients receiving hydroxyurea therapy during the chronic phase of chronic myelogenous leukemia [3].
• All had orthostatic edema and varicose veins, but leg ulcers and other "postphlebitic" sequelae were infrequent [4].
• In prolidase deficiency, the characteristic skin manifestations are inflammatory indurations and chronic leg ulcers [5].

High impact information on Leg Ulcer

• In addition, the leg ulcer healed; his WBC count, hemoglobin level, temperature, ESR, and weight returned to normal; the rheumatoid factor titer dropped substantially; and the antinuclear antibodies disappeared [6].
• Pentoxifylline for treatment of venous leg ulcers: a systematic review [7].
• Five consecutive patients with cryofibrinogenaemia in association with painful leg ulcers and intravascular dermal thrombi were treated with stanozolol, an androgenic steroid with fibrinolytic properties [8].
• Topical prostaglandin E2 for chronic leg ulcers [9].
• Wound healing produced by isotonic saline irrigation via a special dressing was compared with that produced by conventional saline dressings in 12 inpatients with 18 leg ulcers [10].

Chemical compound and disease context of Leg Ulcer

• Letter: Zinc-65 retention in patients with stasis leg ulcers [11].
• Hydroxyurea-induced leg ulcers treated with Apligraf [12].
• L-carnitine for leg ulcers [13].
• Accelerated healing of chronic sickle-cell leg ulcers treated with RGD peptide matrix. RGD Study Group [14].
• Pyruvate kinase deficiency and leg ulcers [15].

Biological context of Leg Ulcer

• Up-regulation of COX-1 in chronic venous leg ulcers could produce prostacyclin, which contributes to angiogenesis [16].
• Venous leg ulcers and apoptosis: a TIMP-3-mediated pathway [17]?
• Our findings support the view that in the acute wound environment the plasminogen activator system is proteolytically active and that in chronic leg ulcers urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor may also be organized for cell adhesion and migration [18].
• The VenUS II trial is the first large, prospective clinical study to investigate the effect of larval therapy and hydrogel on both the bacteriology and healing of leg ulcers [19].
• PATIENTS AND METHODS: To stimulate fibrinolysis, tissue type plasminogen activator (t-PA) containing ointment was applied over 12 weeks on chronic venous leg ulcers of six patients [20].

Anatomical context of Leg Ulcer

• Serine proteinase activities were low in leg ulcer exudates but very high in some but not all acute wound fluids [21].
• These results suggest that serine protease activity in leg ulcer fluid degrades plasminogen and support the hypothesis that keratinocyte migration may be impaired in leg ulcers because of a reduced availability of intact plasminogen for plasmin generation [22].
• The mutations 4 and 6 have been found in 66% of alleles of WS cases in Japan. The increased frequency and unusual age and site distributions of OS in WS may be due to increased susceptibility, related to later-life leg ulcers, and weight-bearing on spindly ankles weakened by severe loss of lower limb subcutaneous tissue [23].
• In healing leg ulcers the alphavbeta3 integrin was predominantly localized around capillary vessels preferentially at sites of newly formed granulation tissue [24].
• Fibroblasts cultured from chronic leg ulcers showed a higher level of FN compared to normal fibroblasts [25].

Gene context of Leg Ulcer

• This study tested the hypothesis that excessive tumor necrosis factor-alpha (TNF-alpha) levels in chronic venous leg ulcers are associated with impaired healing [26].
• Fibrin zymography showed significantly elevated endogenous uPA activity in venous leg ulcers in comparison with healthy controls [27].
• Elevated expression of extracellular matrix metalloproteinase inducer (CD147) and membrane-type matrix metalloproteinases in venous leg ulcers [28].
• The impact of differential expression of extracellular matrix metalloproteinase inducer, matrix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase-2 and PDGF-AA on the chronicity of venous leg ulcers [29].
• The terminal complement complex is generated in chronic leg ulcers in the absence of protectin (CD59) [30].

Analytical, diagnostic and therapeutic context of Leg Ulcer

• Wound fluid samples from chronic leg ulcers in nonhealing and healing phases and wound fluid from mastectomy wounds were assayed for ferritin, transferrin, total iron, 8-isoprostane, and total antioxidant status [31].
• METHODS: We performed a randomized, placebo-controlled, single blind study in which 87 patients who had venous leg ulcers homogeneous for dimensions and characteristics were treated for 20 days with an infusion of prostaglandin E-1 or placebo, in association with topical therapy [32].
• Adverse effects associated with EMLA cream used as topical anesthetic for the mechanical debridement of leg ulcers [33].
• Proteolytic inactivation of transforming growth factor beta3 by elastase in venous leg ulcers: implications for clinical trials using topically-applied peptide growth factors [34].
• Methods Patients with nonhealing venous leg ulcers were treated with intradermal injection of recombinant human GM-CSF, and biopsies were taken at the ulcer margin before and 5 days after administration [35].

References