Disease relevance of Varicose Ulcer

• The interference of hyperglycemia with hypoxia-dependent stabilization of HIF-1alpha protein levels was confirmed in vivo, where only very low levels of HIF-1alpha protein could be detected in diabetic wounds, as compared with chronic venous ulcers [1].
• Thus, inhibition of COX-1 by non-steroidal anti-inflammatory drugs (NSAIDs) could increase the local ischaemia and hypoxia associated with chronic venous ulcers [2].
• Micronised purified flavonoid fraction: a review of its use in chronic venous insufficiency, venous ulcers and haemorrhoids [3].
• The indications for these studies were leg pain (34%), leg swelling (24%), surveillance for DVT in a patient at high risk (23%), searching for a source of pulmonary embolism (14%), follow-up of previously diagnosed DVT (3%), and other indications (i.e., varicose veins, venous ulcer, 2%) [4].
• RESULTS: TGF-beta3 expression was increased in the epithelium at the edge of diabetic foot ulcers, being more intense than diabetic and normal skin (P = 0.03, 0.02, respectively), as was its expression in venous ulcers compared with normal skin [5].

Psychiatry related information on Varicose Ulcer

• No studies evaluating topical phlebotonics, chromocarbe, naftazone or disodium flavodate fulfilled the inclusion criteria.Outcomes included oedema, venous ulcers, trophic disorders, subjective symptoms (pain, cramps, restless legs, itching, heaviness, swelling and paraesthesias), global assessment measures and side effects [6].

High impact information on Varicose Ulcer

• Sucralfate and chronic venous stasis ulcers [7].
• Sequential changes in histologic pattern and extracellular matrix deposition during the healing of chronic venous ulcers [8].
• De novo appearance of COX-2 in chronic venous ulcers was demonstrated, which is not seen in normal human skin [2].
• Expression of cyclooxygenase isoforms in normal human skin and chronic venous ulcers [2].
• The results demonstrated an increased distribution of both NOS and arginase in chronic venous ulcer tissue compared with normal skin, with inflammatory cells and vascular endothelial cells as the main sources [9].

Chemical compound and disease context of Varicose Ulcer

• NO overexpression in chronic venous ulcers may be involved directly or indirectly (through production of peroxynitrite) in the pathogenesis and delayed healing of chronic venous ulcers, through its effects on vasculature, inflammation, and collagen deposition [9].
• No leakage occurred following gamma sterilization of the dressing and, more importantly, the deferoxamine-coupled cellulose dressing retained its iron complexing properties sufficient to reduce iron levels found in chronic venous ulcers to levels comparable to those found in acute wounds [10].
• The good long-term results in 78% of the cases indicate that patients with recurrent venous stasis ulcers may receive lasting benefit from modified Linton procedures [11].
• When tissue samples were subjected to fibronectin zymography, the main protease involved in the breakdown of fibronectin in both venous ulcers and acute wounds of elderly subjects was found to be a serine protease with a molecular weight of approximately 30 kd [12].
• Topical application of povidone-iodine in the management of decubitus and stasis ulcers [13].

Biological context of Varicose Ulcer

• Expression of FN, CS, and TN was detected in dermal tissue early in normal wound healing (5-19 d p.w.). Abundant staining was seen 3 mo p.w., returning to prewounding levels after 12-18 mo p.w. In the dermis of chronic diabetic and venous ulcers with a duration of 12 mo or more, a prolonged presence of these ECM molecules was noted [14].
• BACKGROUND: Fibroblasts (fb) cultured from venous ulcer patients and patients with venous reflux disease without ulcer demonstrate characteristics of cellular senescence, such as increased fibronectin level and senescence-associated beta-galactosidase (SA beta-gal) positive cells [15].
• Mitogen-activated protein kinase pathway regulates cell proliferation in venous ulcer fibroblasts [16].

Anatomical context of Varicose Ulcer

• We conclude that venous ulcer edge-derived fibroblasts have an impaired ability to synthesize collagen in vitro, but synthesize fibronectin normally [17].
• RESULTS: Venous ulcer exudates significantly inhibited angiogenesis (mean (95 per cent confidence interval) 0.72 (0.48 to 0.96)) compared with acute wound fluids (2.48 (0.86 to 4.10)) (P < 0.002) and VEGF (1.47 (1.32 to 1.61)) (P = 0.01) [18].
• BACKGROUND: To determine the results of standardized ulcer treatment regimes and effects of the oral thromboxane A2 antagonist Ifetroban (250 mg daily) on healing of chronic lower-extremity venous stasis ulcers [19].
• Infrainguinal bypass grafting with saphenous vein evolved in clinics set up to treat varicose veins and varicose ulcers [20].

Gene context of Varicose Ulcer

• The levels of soluble p55 and p75 receptors in wound fluid showed a significant linear correlation (p < 0.001), suggesting a partially coordinated or common regulatory mechanism for the cleavage of transmembrane TNF receptors in chronic venous ulcers in vivo [21].
• CONCLUSION: In nonhealing venous ulcers there is a consistently high level of expression of VEGF, at both the gene transcript and protein level [22].
• CONCLUSION: Non-healing venous ulcers are associated with greater activity MMP-2 activity [23].
• A significantly higher ratio of TCC/CD59 was found in the ischaemic compared to venous ulcers (p = 0.018) [24].
• We conclude that venous ulcer fibroblasts show decreased Type II receptor expression and display abnormalities in the downstream signaling pathway involving MAPK and the early Smad pathway [25].

Analytical, diagnostic and therapeutic context of Varicose Ulcer

• In situ hybridization was performed to localize collagenase, stromelysin-1, stromelysin-2, matrilysin, urokinase plasminogen activator (uPA) and TIMP-1 mRNAs in 14 chronic venous ulcers and 10 normally healing wounds, representing different time points after wounding [26].
• The aim of this study was to determine the local venous levels of VEGF and TNF(alpha) in limbs with venous ulcers before and after treatment with graduated compression [27].
• Prevalence, incidence, management, and predictors of venous ulcers in the long-term-care population using the MDS [28].
• Sclerotherapy for varicose veins. Treatment prevents stasis ulcers and other complications [29].
• Subfascial endoscopic ligation of perforator veins (SEPS) in the treatment of venous ulcers [30].

References