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1.
J Am Coll Clin Wound Spec ; 6(3): 32-7, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27104143

RESUMO

In order to assess the impact of comorbidities and identify factors that accelerate the healing rate of venous leg ulcers we performed an extensive, retrospective analysis of our experience in a diverse population. From June, 2006 to June, 2014, 897 patients with 1249 venous leg ulcers were treated at Lake Wound Clinics. Treatment protocols utilized the standard regimen of wound cleaning, debridement and compression bandaging. Wound cleaning, autolytic debridement, packing and dressing of venous leg ulcers utilized aqueous solutions of hypochlorous acid (HCA) rather than the standard normal saline. This protocol caused all ulcers to close completely. Comorbidities that delayed healing included uncontrolled or poorly controlled diabetes mellitus, advanced peripheral artery occlusive disease (PAD), active smoking, use of steroid medications and/or street drugs, large initial ulcer size and significant depth. Other factors, including advanced age, recurrent venous ulceration, stasis dermatitis, lipodermatosclerosis, morbid obesity and infection with one or more multidrug resistant organisms did not delay closure. From this experience we conclude that venous leg ulcer care protocols that clean, debride, pack and dress with hypochlorous acid solutions can reduce the effects of some comorbidities while accelerating healing times. Additional benefits are described.

2.
Int Wound J ; 4(3): 241-50, 2007 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-17924880

RESUMO

For the past 20 years, super-oxidised solutions (SOSs) have been shown to be potent antimicrobials and disinfectants via oxidative damage. However, the potential toxicity of SOSs on eukaryotic cells has not been documented in vitro. This is relevant because oxygen and chlorine reactive species may possibly induce ageing and irreversible cellular dysfunctions that eventually produce cell death. The present study investigates the cytotoxicity and oxidative stress induced by a novel, pH-neutral SOS (i.e. Microcyn, MCN) on young, primary diploid - human dermal fibroblast (HDF) cultures. For this purpose, hydrogen peroxide (HP) was used as a positive control of oxidative damage. When these solutions were used at concentrations indicated for wound care (i.e. undiluted MCN or 880 mM HP), HP was significantly more toxic than MCN. After 5 and 30 minutes of exposure, cell viability was 38% and 5%, respectively, in 880 mM HP-treated cells versus 75% and 70% in MCN-treated populations, respectively. HP induced both apoptosis and necrosis, whereas MCN induced only necrosis. Genotoxic and ageing studies were then conducted at sublethal HP concentrations as previously reported in the literature. Cellular DNA and RNA were partially degraded only in HDFs exposed to 500 microM HP for 30 minutes but not in those exposed to undiluted MCN. At this same concentration, HP induced the formation of 8-hydroxy-2'deoxyguanosine adducts in HDFs but this effect was neither observed in control- nor observed in MCN-treated cells. HDFs were further exposed to 5 microM HP or 10% MCN for 1 month. The expression of senescence-associated-beta-galactosidase was only significantly elevated in cells chronically exposed to 5 microM HP. Altogether, these results show that MCN is significantly less cytotoxic than antiseptic HP concentrations (i.e. 880 mM) and that, in vitro, it does not induce genotoxicity or accelerated ageing.


Assuntos
Desinfetantes/farmacologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/patologia , Peróxido de Hidrogênio/farmacologia , Pele/citologia , 8-Hidroxi-2'-Desoxiguanosina , Anti-Infecciosos Locais/farmacologia , Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Adutos de DNA/efeitos dos fármacos , Dano ao DNA/efeitos dos fármacos , Desoxiguanosina/análogos & derivados , Desoxiguanosina/metabolismo , Humanos , Concentração de Íons de Hidrogênio , Necrose/induzido quimicamente , Estresse Oxidativo/efeitos dos fármacos , Estabilidade de RNA/efeitos dos fármacos , beta-Galactosidase/metabolismo
3.
Angiology ; 57(2): 139-44, 2006.
Artigo em Inglês | MEDLINE | ID: mdl-16518520

RESUMO

The etiologies of venous leg ulcers have been well known for millennia, and yet there remains no simple solution to this very common problem. Achieving closure of venous leg ulcers is often a lengthy process that is further complicated by the presence of significant comorbidities. The authors present data on healing venous leg ulcers in a cohort of 231 patients, most of whom had 1 or more complicating factors. Our multidisciplinary and aggressive approach to healing venous leg ulcers is described and has resulted in an average healing time of 29 days, a significantly shorter duration of treatment than the reported average of 6 months.


Assuntos
Antibacterianos/uso terapêutico , Desbridamento/métodos , Oxigenoterapia Hiperbárica/métodos , Curativos Oclusivos , Úlcera Varicosa/terapia , Cicatrização , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Resultado do Tratamento , Úlcera Varicosa/patologia
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